Furthermore, in light of recent findings on JAK1 and JAK2 inactivating mutations as a genetic mechanism for innate as well as acquired resistance to anti-PD1 in melanomas [35, 36], our results suggest JAK2 activating mutations may serve as a marker for response to both JAK inhibitors and anti-PD1 immunotherapy in NSCLCs. The gene discussed is JAK2; the disease is melanoma.