Indeed, the attempts to re-adjust the levels of H4K16Ac using TSA slowed 53BP1 accumulation to damage sites in both the RSC316 and RSC526 resistant clones, but not parental CRC cells, without affecting the initial number of γH2AX foci (Figure 6C, Figures S11C and S12B). This evidence concerns the gene TP53BP1 and colorectal carcinoma.