Multiple independent studies also supported inhibitory polyphenolic effects on melanoma cells viability through upregulation of p53 and/or regulation of its downstream proapoptotic and anti-apoptotic effectors, such as BAX and BID or BCL-2, BCL-XL, and MCL-1, respectively, accompanied with elevated levels of cleaved caspases of intrinsic or extrinsic apoptotic pathways [57,62,69,71,72,73]. Here, BCL2 is linked to melanoma.