Current research has revealed at least three mechanisms: (1) Downregulation of JAK/STAT signaling, preventing interferon-γ (IFN-γ)-induced PD-L1 upregulation 20; (2) Suppression of EGFR signaling, promoting PD-L1 ubiquitination and degradation, thereby enhancing CD8+ T and natural killer (NK) cell infiltration and cytotoxicity 20; (3) Targeting phosphatidylserine (PS) on cancer cells, suppressing PD-L1 and strengthening T cell-mediated immunity 39. The gene discussed is SOAT1; the disease is cancer.