Collectively, these data led to a model proposing that the hyper-activation of IL7/IL7R signaling (JAK/STAT pathway) can increase the expression of the anti-apoptotic BCL2 protein through the accumulation of H3K27ac active marks at an enhancer (e.g. Bcl2 + 105Kb) bound by STAT5b, and this can play an antagonistic role to LSD1i that reactivates the expression of pro-apoptotic genes, which are normally repressed by the ZEB2/LSD1/NuRD complex in the context of Zeb2Tg ETP-ALL. Here, SOAT1 is linked to acute lymphoblastic leukemia.