[38]) T-ALL, consistent with this gene triad being direct targets of activation by MEF2C [83]. Nonetheless, LYL1 and LMO1/2 expression was detected in a majority of T-ALL samples independently of MEF2C or of phenotypic classification and included TLX1/3- and HOXA9-expressing leukemias (Fig. 6C and S11 Fig.). These observations suggest that the molecular pathways controlling self-renewal described here is not limited to T-ALL samples harboring TAL1 or LMO1/2 translocations but may be relevant to other oncogenic subtypes of T-ALL. This evidence concerns the gene LYL1 and leukemia.