Previous work is focused on the relationship between AML with oncogenes, such as Bcl-2 (Pan et al., 2017) and EGFR (Mahmud et al., 2016), with tumor suppressor genes, such as p53 (Pan et al., 2017), and with Bcl-2 homology domain 3 (BH3)-only proteins, such as Puma, Bim, and Noxa (Bilardi et al., 2016; Grundy et al., 2018). The gene discussed is BCL2; the disease is acute myeloid leukemia.