ANGPTL2 and renal cell carcinoma associated with Xp11.2 translocations/TFE3 gene fusions: 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).