RALD is characterized by persistent monocytosis; often associated with leukocytosis, lymphoproliferation, and autoimmune phenomena, early onset (mostly at the age <5 years old), and resistance to IL2 depletion-dependent apoptosis; and caused by somatic mutations in RAS genes (NRAS and KRAS), which plays an important role in intracellular signaling and control proliferation and apoptosis (204, 206, 207). This evidence concerns the gene NRAS and Increased total leukocyte count.