Our results indeed show ITH for this group of clinically relevant CNVs, with a significant overrepresentation of chr8p deletion (p < 0.001), chr9p deletion (p < 0.001), and chr22q deletion (p = 0.014) among regions corresponding to SETD2 wt tumors (Fig. 6B), suggesting that the presence of SETD2 mutation/loss of H3K36me3 influences genomic stability or drives tumor development down a more epigenetically driven pathway less reliant on genome instability. The gene discussed is SETD2; the disease is neoplasm.