HDAC2 and cancer: Given the relatedness of the gene signature of embryonic stem and cancer cells [32, 36] and the fact that epigenetic modifications may change with each division of a cell carrying a tumoral translocation [58], we can imagine that, in our model, the chance of the daughter cell progressing to RC or remaining ML at each cycle greatly depends on the interplay of proteins (YY1, c-MYC and HDAC2) in concert with the enrichment of the activated fast cell cycle/stemness genes and the silenced differentiation/slow cell cycle genes in the case of RC, or vice versa in the case of ML (see Figure 3E).