In their study, Smith et al. analyzed a morphologically diverse cohort of AML patients and observed a specific expression profile of CBFA2T3::GLIS2-positive patients with disruption of NCAM1 (Neural Cell Adhesion Molecule 1) (CD56), CACNB2 (Calcium Voltage-Gated Channel Auxiliary Subunit Beta 2) and GABRE (Gamma-Aminobutyric Acid Type A Receptor Epsilon Subunit) genes [13]. This evidence concerns the gene CACNB2 and acute myeloid leukemia.