This latter idea is consistent with the moderately increased incidence of cancer in patients with RASopathy, with the spontaneous regression of the JMML-like MPN that develops in some infants with NS and with molecular analyses showing that, when patients with germline HRAS mutations develop sarcomas, these tumors frequently exhibit somatic uniparental disomy with duplication of mutant HRAS and loss of the corresponding normal allele (4, 7, 38, 39). This evidence concerns the gene HRAS and juvenile myelomonocytic leukemia.