STAT1 and neoplasm: This model exhibited a significant increase in colon tumor incidence, underscoring the crucial role of the APC C terminus in tumorigenesis.38 The majority of APC mutations (~90%) result in premature stop codons, leading to truncated proteins that lack both the C-terminal PTPN13-binding domain and the regions responsible for β-catenin regulation.35,39,40 As a result, APC mutations simultaneously activate Wnt/β-catenin signaling, promoting tumor proliferation, while also impairing the IFNγ-STAT1-IRF1-MHC class I antigen presentation pathway, promoting immune evasion.