Various cellular mechanisms have been proposed to explain the role of PrP in cancer cells, including the activation of PI3K/Akt signaling pathway to up-regulate cyclin D in gastric cancer cells [9], chemotherapy drug induced PrP interaction with P-glycoprotein (P-gp, ATP-dependent drug-efflux pumps ABCB1) in a drug-resistant MCF7 breast cancer subline [15], and the presence of an aberrantly processed pro-PrP form that disrupts normal cell physiology by binding to filamin A in melanoma and pancreatic cancer cells [12], [13]. This evidence concerns the gene PRNP and melanoma.