USP28 is more implicated in cancer than US25, as it has a larger number of onco-proteins on its client list, including prominent ones like c-MYC (45), MYCN (46), LSD1 (47), etc. Now, with the identification of KRAS here as dependent on USP25 for its expression, the USP25/28 dual are gaining more importance as targets for cancer therapy, since their inhibition can now simultaneously suppress both c-MYC and KRAS (Fig. 4, C and D), the two most prominent onco-drivers. The gene discussed is KDM1A; the disease is cancer.