For instance, genetic alterations in transcription factor CCAAT/enhancer binding protein α (C/EBPα) drives the onset of AML both in mice and in humans [91], while the promyelocytic leukemia-retinoic acid receptor α (PML-RARα) fusion protein (i.e., the product of the balanced translocation t(15;17)) represents the main oncogenic driver of the acute promyelocytic leukemia (APL) AML subset [92]. The gene discussed is CEBPA; the disease is acute myeloid leukemia.