In tumor cells, CRISPR loss-of-function of PTPN2 amplifies IFN-γ-STAT1 signaling and upregulates CXCL9/10/11 and CCL5, which increases T-cell recruitment and sensitizes tumors to adoptive T-cell therapies; complementary CRISPR deletion of PTPN2 in engineered T cells enhances effector function and persistence, providing a bidirectional route to boost trafficking and function in solid tumors 145. The gene discussed is STAT1; the disease is neoplasm.