It has been shown, in colon carcinoma-derived cells, that the FOXO system activation/inhibition via gene overexpression/silencing or the pharmacological perturbation of several signalling pathways (PI3K-AKT, Wnt, β-catenin, EGFR) lead to CRC cancerogenesis [86–115]. The gene discussed is EGFR; the disease is colorectal carcinoma.