Establishing a stepwise model of congenital neutropenia to acute myeloid leukemia (AML), derived from congenital neutropenia patient-derived iPSCs by CRISPR/Cas9, revealed that BAALC and MK2a phosphorylation may be excellent targets for preventing leukemogenic transformation or eliminate AML blasts [39]. This evidence concerns the gene BAALC and severe congenital neutropenia.