Success in targeting melanomas with RAS mutations may be achieved by inhibiting RAS effector pathways through combined targeting of BRAF, MEK, and PI3K/AKT/mammalian target of rapamycin (mTOR) due to the integral role of these effectors in RAS driven transformation as well as the availability of clinically tested small molecule inhibitors (Davies et al., 2007; Engelman et al., 2008; Fasolo and Sessa, 2008; Lee et al., 2010; Gysin et al., 2011). This evidence concerns the gene AKT1 and melanoma.