The activation of and dependence on ERK signaling are consistent with the high levels of inflammation observed in mice with KRAS mutations, leukemic monocytes from patients with KRAS mutations (66), inflammatory disease in patients with CMML (which is frequently RAS driven), and our data on PBMCs from PTPN11-JMML patients (Figure 2A). The gene discussed is KRAS; the disease is juvenile myelomonocytic leukemia.