To assess relevance of these mechanisms to ANGPTL2‐mediated MHC‐I repression in tRCC cells, we assessed levels of H3K27me3 and tri‐methylation of histone H3 lysine 4 (H3K4me3), the latter an active gene expression mark, at the H2‐K1 and Tap1 promoters in IFNγ‐treated control, Angptl2 KO, and Itgα5 KO tRCC cells using ChIP (Fig. 4C). The gene discussed is TAP1; the disease is renal cell carcinoma associated with Xp11.2 translocations/TFE3 gene fusions.