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. This evidence concerns the gene MC1R and neoplasm.