Specifically, in shCBX2 cells, we observed the upregulation of several MAPK phosphatases, including members of the dual-specificity phosphatase (DUSP) family such as DUSP5 and DUSP10, which preferably dephosphorylate ERK and p38, respectively, and the downregulation of KRAS and IL-1β, a key mediator of cell expansion and disease progression in AML following p38 MAPK activation [23] (Fig. 5C and Fig. 6 A, B). The gene discussed is IL1B; the disease is acute myeloid leukemia.