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]. This evidence concerns the gene TP53 and acute myeloid leukemia.