Figure 8B shows that MPE treatment induced a consistent increase in γH2AX level as well as in the phosphorylated ATM protein (pATM) in all colon cancer cells, suggesting the recruitment of this repair system at DNA breaks. On the other hand, the involvement of the above-mentioned stress proteins as players correlated to γH2AX increase cannot be excluded. In fact, beyond pATM, H2AX phosphorylation could also be ascribed to other kinases such as pJNK [39], which in our experimental conditions was upregulated by MPE treatment (Figure 6), or the phosphorylated form of the kinase p38 [40]. This evidence concerns the gene H2AX and colonic neoplasm.