Suppression of HDACs in vemurafenib-resistant PDX BRAFV600E melanoma cells, improved cell killing in combination with dabrafenib and trametinib, including non-apoptotic mechanisms, inactivation of AKT, mTOR, and MEK1/2-ERK1/2, activation of CD95 death receptor and autophagy, dysfunctional mitochondria leading to cell death. This evidence concerns the gene AKT1 and melanoma.