Notably, most JMML patients inherit a heterozygous mutation in CBL or one of a small set of other genes (such as NF1, N-Ras, PTPN11) that regulate RAS signaling, constituting one form of RASopathies [5, 11], with the disease progression invariably associated with a somatic duplication of the mutant allele and concurrent deletion of the wildtype allele in hematopoietic stem cells, referred to as acquired uniparental disomy [7]. Here, PTPN11 is linked to juvenile myelomonocytic leukemia.