De facto, these genetic lesions occur temporally following the founder mutations [25], and confer proliferative advantages to tumor cells by impairing normal apoptotic activity compromising the function of FMS-like tyrosine kinase 3 (FLT3) [10], neuroblastoma RAS viral oncogene homolog (NRAS) [26], nucleophosmin (NPM1), and TP53 [27, 28]. Here, NPM1 is linked to neoplasm.