In contrast, inferred activity of this pathway increased starkly to become dominant in C3HeB/FeJ mice at 20 days after infection (Fig. 4 b), driven by high predicted signaling activity of Cxcl2 between neutrophils, as well as from the macrophage/monocyte 1 and 2 clusters to neutrophils (Fig. S2 a). The gene discussed is CXCL2; the disease is infection.