Thus, the data presented here suggest a more general role for LMO2 to shape the epigenome or to be involved in chromatin remodeling early on in T‐ALL disease and it would not be surprising that other important drivers for human T‐ALL, like SCL, LMO1, or HOX11/TLX1, contribute to the neoplasm through a similar reprogramming mechanism. Here, TLX1 is linked to acute lymphoblastic leukemia.