JAK1 and melanoma: Recent studies have reported that inactivating mutations of JAK1/2 are associated with resistance to PD-1 blockade in melanoma [27–29], whereas genetic inhibition of the JAK-STAT pathway results in resistance to anti-PD-1 therapy [30], suggesting that the complete response to our salvage therapy was mainly due to the combined effects of ruxolitinib and chidamide but not PD-1 blockade.