Altered gene function in AML is often a consequence of distinct cytogenetic aberrations [4], but also results from mutations in genes like CEBPA (CCAAT/enhancer-binding protein, alpha), FLT3 (fms-like tyrosine kinase receptor-3), or NPM1 (nucleophosmin 1) [3,4]. Here, CEBPA is linked to acute myeloid leukemia.