A recent low-copy transposon mutagenesis screening methodology in mice identified Map3k1 as a potentiator of melanoma.69 Point mutations within introns 9 and 10 of Map3k1 produce truncated forms of Map3k1 that lack the N-terminal regulatory region.69 N-terminal truncation of Map3k1 leads to enhanced Mapk1/3 phosphorylation in melanoma tumors, and provides a possible mechanism to explain how Map3k1 may drive malignancy in melanoma.69 It is also notable that host immunodeficiency may also contribute to the prognosis of Map3k1-dependent cancers.70 This evidence concerns the gene MAP3K1 and cancer.