Some authors have hypothesized that Shp-2-mediated STAT3 hypophosphorylation might also have a role in the phenotypic abnormalities observed in NS and/or during the pathogenesis of JMML.22 Contrary to the results by Zhang et al., we did not observed any altered pattern of STAT3 phosphorylation in our series of PB cells from RAS-mutated patients. This evidence concerns the gene STAT3 and juvenile myelomonocytic leukemia.