Although IFN-γ activates both STAT1 and STAT3, how these pathways interact to regulate immune evasion under hypoxia remains unclear.<h4>Methods</h4>Using the MC38 murine colorectal cancer model and T cell-tumor spheroid co-culture assays, we examined how IFN-γ signaling through STAT1 and STAT3 regulates PD-L1 expression, CSC plasticity, and cytotoxic T cell function under normoxic and hypoxic conditions. This evidence concerns the gene STAT3 and neoplasm.