In most MPN cases, genetic defects mainly concern acquired somatic mutations involving Janus kinase 2 (JAK2) [5,6,7,8,9], thrombopoietin receptor (MPL) [10,11], or calreticulin (CALR) genes [12,13], which affect JAK-STAT (signal transducers and activators of transcription) signaling pathways, with JAK2 and STAT5 being the ultimate players, as well as JAK-related pathways PI3K/AKT and Ras/MAPK [5,12,14,15,16,17,18]. This evidence concerns the gene AKT1 and myeloproliferative disorder.