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. Here, SOAT1 is linked to melanoma.