This adaptor activity of SHP2 and the inhibitory role of CBL in the regulation of GRB2-SOS complex function illustrate how CBL loss-of-function mutations and PTPN11 gain-of-function mutations (through the adaptor activity of SHP2) functionally converge through a similar molecular mechanism to induce RAS activation, which could explain why these two genetic alterations are mutually exclusive in JMML [42]. This evidence concerns the gene PTPN11 and juvenile myelomonocytic leukemia.