Our results demonstrate that: 1) loss of JAK1 induces T-cell resistance in tumor cells in vitro and in vivo; 2) both type I and II IFN pathways are impaired in the absence of JAK; 3) JAK1-deficient tumor cells are resistant to type I and II IFN-induced apoptosis; 4) T-cell activation is compromised in tumor cells lacking JAK1; and 5) exogenous type I IFN can induce regression of JAK1-deficient tumors by activating host non-tumor immune cells (Figure 7). Here, IFNA1 is linked to neoplasm.