On the other hand, AKT inhibition decreased mTORC1 activity in all the CR melanoma cells lines tested, suggesting that AKT is upstream of mTORC1 activity in cells with mutant or wild-type PTEN. These results are consistent with the findings that the activation of PI3K/AKT pathway is crucial in the acquisition of drug resistance in melanoma [74, 76, 77]. This evidence concerns the gene AKT1 and melanoma.