In this study we investigated the molecular mechanisms underlying azacitidine and lenalidomide therapy, focusing on the mutation profile of cancer myeloid genes (i.e., ASXL1, RUNX1, TET2, IDH1/2) as well as a selection of inositide-related genes, known to be involved in survival pathways (i.e., PI3K/Akt/mTOR, RAS/MAPK), hematopoietic differentiation (i.e., protein kinase C alpha, PI-PLCgamma2) [21], cell cycle (i.e., CDKN2B, protein kinase C alpha) [57] or drug metabolism (i.e., RPS6KA3, SOD2, CYP2D6, SLC29A2). Here, CDKN2B is linked to cancer.