A recent study showed that the genetic silencing of all AKT paralogs induced melanoma cell death [41], although, in that case, an mTOR pathway downstream of AKT was implicated, as opposed to our findings, which implicated the AKT depletion-mediated dephosphorylation of BAD, which increased BAD-mediated apoptosis, given that navitoclax, a Bcl2 inhibitor, could substitute for CD133 or AKT depletion [5]. This evidence concerns the gene PROM1 and melanoma.