Recently, clonal hematopoiesis (CH), disrupting epigenetic regulators in the majority of BPDCN cases, was proposed as an underlying mechanism rendering mutations in RAS signaling (NRAS, KRAS) and tumor suppressors like TP53 and ATM secondary clonal events and thereby more specific in BPDCN pathogenesis [44]. The gene discussed is NRAS; the disease is CD4+/CD56+ hematodermic neoplasm.