Unfortunately, although several FTase inhibitors (FTIs) showed great anti-tumor potency in preclinical studies, phase II and phase III clinical trials on solid tumors showed resistance to FTIs.364–366 One explanation provided for this disappointing failure is that KRAS and NRAS mutations are susceptible to alternative prenylation mediated by geranylgeranyltransferase-I (GGTase-I) which promotes RAS membrane localization and oncogenic activation when FTase is blocked.365,367,368. This evidence concerns the gene KRAS and neoplasm.