Restoration of AKT phosphorylation by insulin, IGF1 and leptin in cells treated with terbinafine plus FMCC was prevented by intracellular cholesterol depletion with MβCD (Fig. 6b), supporting the notion that the effect of supplemented insulin, IGF1 and leptin on AKT activation (in cells treated with FMCC plus CBIs) reflects their ability to increase cholesterol content inside the cancer cell. This evidence concerns the gene AKT1 and cancer.