The mechanisms of primary as well as acquired resistance to ICI are incompletely understood but include inadequate T cell infiltration into the tumor [1], immunosuppressive factors within the tumor microenvironment (TME) [1,2], loss of T cell function through the expression of alternative immune checkpoints [3], disruption of interferon gamma signaling via JAK1/2 mutations [4,5], impaired antigen presentation and neoantigen loss [5,6]. Here, JAK1 is linked to neoplasm.