RIPK3 has been found to be epigenetically silenced in breast and pancreatic cancer tissue14, 15 and in melanoma cell line.16 In tumor models, loss of RIPK3 aided a TAK1-induced inflammation model of hepatocarcinogenesis,17 whereas loss of RIPK3 in combination with internal tandem duplication mutations of FMS-like tyrosine kinase-3 led to an increase in leukemia in vivo, which was because of the absence of inflammasome activation.18 Expression of RIPK3 in patient samples also has been associated with disease outcome. This evidence concerns the gene RIPK3 and melanoma.