Damage-responsive, maturity-silenced enhancers regulate multiple genes that direct regeneration in <i>Drosophila</i>.

This mechanism is likely to be significant for some genes, but it is difficult to make clear statements regarding the number of genes that might be regulated in this way. 2) If chromatin accessibility is still considered an important indicator of damage responsiveness, please explain why the 5% of genes overlapping with gene expression data are not followed up as a set of interesting genes, and also why they do not follow up with the 28 potential DRMS enhancers defined by chromatin accessibility criteria?

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