Guest Blog Series 2026

By Hemlata Pant

I first came across epigenetics at A level. Back then, it felt reassuringly neat. I learned that adding chemical tags to DNA or histones could tighten or loosen chromatin, and that this helped control whether genes were active or silent. The logic held together, the diagrams were tidy, and it all felt reasonably contained.

But there’s a difference between following diagrams and really understanding them. Where there are molecules (especially biomolecules) complexity and nuance always seems to follow.

The more time you spend with chromatin biology, the more you realise that these mechanisms almost never act in isolation. The same epigenetic mark can mean different things in different contexts. Effects depend on timing, cell type and what else is happening around it. Epigenetics, it turns out, is less about switches and more about combinations. Meaning only emerges when you look at the wider picture.

I did understand this in my lectures, but it stuck properly somewhere I’d never thought it would: a drug‑development safety meeting at my industrial placement.

In a nutshell, this meeting had lots of lead scientists present, all from slightly different functions, doing a routine talk-through of various safety signals from a drug. This wasn’t a meeting where I was presenting or making decisions, so I was able to truly process how scientists talked through uncertainty. What counted as strong evidence? What was suggestive rather than decisive? What needed action now, and what needed more time?

What surprised me was how familiar the reasoning felt.

In epigenetics, no single signal tells the whole story. A histone modification associated with repression doesn’t automatically switch a gene off. DNA methylation doesn’t act alone. To give meaning to that information, we need to examine the context: the expression data, the chromatin structure, the timing – all of it.

That same logic guided the meeting. Individual findings weren’t treated as answers in themselves. Data from different sources were weighed together, and inconsistencies weren’t rushed away. Some issues were monitored without being escalated, not because they didn’t matter, but because there wasn’t enough evidence yet to justify acting. Meaning only emerges when you look at the wider picture.

This specific idea, tracking without reacting, felt unfamiliar at first. At school and university, we’re often trained to believe that noticing something means you should immediately explain or fix it. I would describe myself as an anxious person, my brain screams “do something!”.

Epigenetics teaches you otherwise. Biology is VERY noisy. Not every signal, it turns out, matters.

And it’s not just a case of “matters/doesn’t matter”. For instance, H3K27ac – an epigenetic modification to the DNA packaging protein histone H3 – is often taught as a straightforward “active enhancer” mark. However, experimental removal of H3K27ac at enhancers in mouse embryonic stem cells (Zhang and Zhang et al., 2020) showed that gene transcription can remain largely unchanged, indicating that enhancer activity does not solely depend on H3K27ac. What this means is that H3K27ac is less like a simple on/off signal and more like one part of a wider chromatin context that has to be read together with other marks and factors. Whether a signal or epigenetic marker “matters” or not, in this case, seems to be context dependent. Meaning only emerges when you look at the wider picture.

Going back to my time in the drug safety meeting, I couldn’t stop thinking about how this related to the mindset training I underwent at uni when studying epigenetics. About how both these topics (drug safety decision making and epigenetics) use the transferable skills of needing to decipher conditional signals, to sit with uncertainty and to resist forcing complicated systems into simple categories. In that “room” (Teams meeting), you could see this play out in real time: toxicologists, clinicians and statisticians all brought slightly different perspectives to the same data, coming together to build a shared, honest picture of what was known and what was still uncertain. Instead of hunting for one decisive result, the discussion circled back to patterns over time, consistency across studies and whether a signal made biological sense in context.

For me, the extended thinking that epigenetics required, at times, was uncomfortable. Just when you think you understand the rules, the certainty starts to slip. But that discomfort, lack of strict categories and extension beyond binary thinking reflects how biology actually works – and how science works outside the classroom. The drug in question is still in development, epigenetics as a field, is indeed, still in development. As an aspiring translational scientist, I am still hoping to contribute to “both” these worlds, though, it may be more appropriate here to remember that this all sits in the beautifully interconnected but complex realm of the life sciences.

Where there are molecules (especially biomolecules and especially epigenetic biomolecules) complexity and nuance always follow. As frustrating as it can get, this friction-laden process of constantly asking why – the most worthwhile one that exists – is what I love the most about science.

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Hemlata Pant is a third-year MSci Biochemistry student with a strong interest in translational science and drug development. She loves writing about all things biochem for her science blog on Substack and is doing her year in industry at GSK, working in Medical Governance at ViiV Healthcare.

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