CHMP5’s function and targets appear to be conserved in mice and humans as DEGs in ICN1-induced murine T-ALL and human NOTCH1-dependent T-ALL lacking CHMP5 include several overlapping genes and pathways highlighted by MYC (Supplementary Fig. 7m, n) and genes that were upregulated in NOTCH-dependent MYC super-enhancer (N-Me)-deficient T-ALL cells (which have diminished MYC expression)17 were also upregulated in the KO T-ALL transcriptome (Supplementary Fig. 7o). The gene discussed is MYC; the disease is acute lymphoblastic leukemia.