However, no available data indicate that PI3K-Akt-mTOR activity is related to specific etiology of the disease, i.e., de novo, secondary or refractory/relapsed AML, nor to specific molecular subtypes, i.e., nucleophosmin 1 (NPM1) or fms like tyrosine kinase 3 (FLT3) mutations or other cytogenetic or molecular genetic alterations [84,85,86]. The gene discussed is NPM1; the disease is acute myeloid leukemia.