As with the Stat3 experiments, the small foci of residual adenocarcinoma remaining in Kmt2a and Dot1l sgRNA orthografts retained target protein expression (Kmt2a/Mll1) or activity (H3K79me2 for Dot1l) (Extended Data Fig. 10b,c), further supporting the critical dependency of ERG-driven cancer on Kmt2a/Mll1 and Dot1l. Interestingly, Men1 (encoding Menin) sgRNA did not impair ERG-dependent tumor growth despite efficient reduction of Menin protein levels in tumors (Fig. 7h and Extended Data Fig. 10d), raising the possibility of ERG/KMT2A cooperativity through a mechanism independent of Menin. This evidence concerns the gene KMT2A and neoplasm.