NPM1 mutations, the most common genetic lesion in AML, abrogate the ability of the protein to localize in the nucleolus and create a new nuclear export signal (NES) at the C-terminus, leading to enhanced nuclear export of mutant NPM1 and its aberrant accumulation in the cytoplasm of leukemic cells [1, 3, 4]. The gene discussed is NPM1; the disease is acute myeloid leukemia.