Taking advantage of the lack of ASIP expression in the B16 melanoma and its sub-lines due to homozygous insertion of a transposable element in the first intron of the a gene encoding ASIP [29], we generated B16-F10 cells stably expressing an ASIP cDNA and compared their colonization, tumor growth and survival outcomes when implanted in syngeneic C57BL/6 mice to that of the parent ASIP-negative B16-F10 cells to investigate a possible role of MC1R in regulating tumor colonization and growth that could be involved in the melanoma risk associated with variants of these proteins. The gene discussed is ASIP; the disease is neoplasm.