Indeed, in a Met-driven transgenic mouse model comprised of tyrosinase-driven rtTA and tet-Met transgenes on the Ink4a/Arf null background (Tyr-rtTA;Tet-Met;Ink4a/Arf−/−, hereafter “iMet”), activation of Met signaling in melanocytes engendered a metastatic melanoma phenotype in vivo (Nogueira C and Chin L, unpublished). The gene discussed is CDKN2A; the disease is melanoma.