Radulovic et al. suggest that the occurrence of additional somatic events, maybe comparable to the PTPN11 gain-of-function mutation c.1508G>T as a driver for juvenile myelomonocytic leukemia (JMML) in their patient 1, may have contributed to the development of specific embryonic tumors, but they did not further speculate on what these events might be specifically in BRCA2-associated malignancies of tissues or organs other than myeloblasts in JMML and how they might be caused. This evidence concerns the gene PTPN11 and juvenile myelomonocytic leukemia.