In this context, whole-exome and RNA sequencing, and reverse-phase protein array data from different the Cancer Genome Atlas (TCGA) datasets (skin cutaneous melanoma, breast invasive carcinoma, lung adenocarcinoma, and colorectal adenocarcinoma) revealed alterations in JAK1 or JAK2 in 5–12 % of the samples, with dependence on cancer type [123]; (iii) crosstalk of JAK/STAT1 signaling with pro-tumorigenic signaling pathways; such as the inhibition of IFN-induced expression of inflammatory genes following STAT3 activation [124]. The gene discussed is STAT1; the disease is cutaneous melanoma.