Previous pan-cancer studies, focusing primarily on SNVs and indels, have identified multiple immune escape mechanisms in immunologically cold tumors, including loss-of-function alterations in antigen presentation genes (e.g., HLA and B2M), PTEN and JAK/STAT alterations, and dysregulation of WNT/b-catenin pathways46,54-56. The gene discussed is SOAT1; the disease is cancer.