Children with CBFA2T3::GLIS2 AML (including AMKL) tend to be younger (median age of onset ∼1.5 years) and display distinct clinical and laboratory features, including stronger expression of CD56 (neural cell adhesion molecule, NCAM) and a more frequent extramedullary involvement compared to other AML (Masetti et al., 2013a; de Rooij et al., 2016; Hara et al., 2017; Smith et al., 2020; Zangrando et al., 2021). The gene discussed is CHL1; the disease is acute myeloid leukemia.