Data from syngeneic mouse models of global host Ccr2 and Il1b gene deficiency and of focal myeloid Ccr2 reconstitution are further supported by human cancer xenograft experiments in Rag2−/− (recombination activating gene 2) mice, which lack B- and T-cell function but feature intact myeloid cells [31], to collectively identify the proposed inflammatory loop that potentiates KRAS blockade. The gene discussed is CCR2; the disease is cancer.