Recent studies have shown that H3K36me3 also participates in cross‐talk with other chromatin marks, including antagonizing H3K4me3 and H3K27me3.[8, 16] Similarly, loss of Setd2 in pancreatic tumor cells triggered a profound decrease in H3K36me3 levels, accompanied by an increase in H3K27me3 levels. The gene discussed is SETD2; the disease is pancreatic neoplasm.