Although our results showing diminished deltarasin efficacy with Il1b−/− mice were less impressive compared with the complete abrogation of deltarasin effects in Ccl2−/− mice, we believe that this is attributable to redundant IL-1α (interleukin-1 alpha) signaling in the former and that targeting IL-1β might be specifically effective against KRAS-mutant cancers [46,47,48,49,50]. The gene discussed is KRAS; the disease is cancer.