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Table 2 Outstanding questions

From: The follicular lymphoma epigenome regulates its microenvironment

1) How do mutations in the epigenetic genes KMT2D, CREBBP and EZH2 (concomitantly or alone) orchestrate and promote the multi-scale (e.g. genetic, molecular, cellular) alterations that drive lymphomagenesis and CPC establishment in FL?
2) What is the clonal evolution of CPC during FL course? How to properly define (in space and time) and target this population?
3) How does FL develop from aberrant GC reactions driven by EZH2 mutant-mediated reprogramming of the microenvironment?
4) How do the epigenetic regulator-TME bidirectional crosstalk interfere with the therapeutic response in FL?
5) Would it be possible to combine epigenetic modifiers that target tumor cells and non-tumor cells in the FL TME? If yes, what combination would be the best for long-term efficacy and complete cure?