The GOF mutant D374Y has increased binding affinity to LDLR, leading to an elevation of LDL-cholesterol in the circulation [47, 103]; D374Y enhances a set of processes relevant to the tumor formation in B16 cells in vitro and B16 cell-derived allografts in vivo along with increases in both esterified and unesterified cholesterol in comparison to wild-type PCSK9. The gene discussed is PCSK9; the disease is neoplasm.