Evi1^high AML cells are dependent on ERG. (A) Relative cell proliferation of EVI1-AML cells expressing shRNAs against Luciferase and Erg in vitro. (B) Colony-forming units of EVI1-AML cells expressing shRNAs against Luciferase and Erg. (C) A Kaplan-Meier survival curve for recipient mice that underwent transplantation with 1 × 10⁶ EVI1-AML cells expressing shRNAs against Luciferase and Erg after being exposed to 6.5 Gy TBI. P value was examined by a log-rank test. (D) Relative cell proliferation of EVI1-AML and KMT2A-MLLT1 clone 1 (CL1) and CL2 cells expressing shRNAs against Luciferase and Evi1 in vitro, showing EVI1-dependency of these cells. (E) Relative cell proliferation of KMT2A-MLLT1 CL2 cells expressing shRNAs against Luciferase and Erg in vitro. (F) Colony-forming units of KMT2A-MLLT1 CL2 cells expressing shRNAs against Luciferase and Erg. (G) Relative cell proliferation of several AML cells and KMT2A-MLLT1-transformed cell lines with shErg compared with those with shLuciferase, through days 0 to 3. A comparison was made within the same original cell between shLuciferase and shErg. (H) A Kaplan-Meier survival curve for recipient mice that underwent transplantation with 1 × 10⁴ KMT2A-MLLT1 AML cells expressing shRNAs against Luciferase and Erg after being exposed to 6.5 Gy TBI. (I) Relative live cell numbers of EVI1-AML cells with shRNAs against Luciferase or Erg treated with daunomycin, compared with those cultured in media without daunomycin. (J) A list of top-ranked gene sets with decreased expression in shErg-transduced EVI1-AML cells. (K) GSEA showing structural constituent of the ribosome is downregulated in shErg. Mean ± SD; ∗P < .05, ∗∗P < .01, ∗∗∗P < .001.