Approximately, 25% of pediatric patients have AML blasts with a normal karyotype, but even these cases often harbor somatic mutations in genes such as WILMS TUMOR 1 (WT1), NPM1, NRAS, KRAS, Fms-like tyrosine kinase 3 (FLT3), and/or c-KIT/CD117 [1, 2]. This evidence concerns the gene NRAS and acute myeloid leukemia.