Overexpression of HOXBLINC in mice enhances hematopoietic stem cell self-renewal and expands myelopoiesis, leading to the development of AML-like disease, reminiscent of the phenotypes seen in the Npm1 mutant knock-in (Npm1(c/+)) mice (Zhu et al., 1956). The gene discussed is NPM1; the disease is acute myeloid leukemia.