Compared with the wildtype gene, four hotspots ANRKD52 mutations (G413W, E506D, S511P and A745T) identified in cancer patient samples (Fig. 5a) failed to effectively rescue the activation defect of STAT1 (Fig. 5b) or upregulation of membrane MHC-I levels (Fig. 5c) upon IFNγ treatment, and thus maintained cancer cell resistance to T cell-mediated killing (Fig. 5d). This evidence concerns the gene STAT1 and cancer.