Whole-exome sequencing of tumor tissues obtained at baseline (before therapy) and after disease progression from four melanoma patients who displayed disease progression after a median 1.8 years objective response to pembrolizumab, revealed that two of the patients exhibited over 90% truncating dysfunctional mutations in JAK1 (Q503* nonsense mutation) and JAK2 (F547 splice‐site mutation), concurrent with the deletion of the wild-type allele and duplication of the mutant allele [43]. The gene discussed is JAK1; the disease is melanoma.