These studies have shown that AEL is largely associated with TP53 mutations (TP53 being a regulator of physiological erythroid differentiation [151]), and mutations commonly found in other types of AML affecting the DNA methylation machinery (e.g., DNMT3A, TET2, IDH), or epigenetic regulators (e.g., KMT2A, NPM1, EZH2, cohesin subunits), and also commonly associate with aberrant expression of CBFA2T3/ETO2, a known GATA1 co-repressor [65,146,147,148,149,152]. The gene discussed is CBFA2T3; the disease is acute erythroid leukemia.