This expansion is dependent on IL-1R signaling: in IL-1R-null mice this process was reduced >50% relative to control (normal mice); interestingly, such mice still mounted a significant inflammatory reaction thus suggesting that the effect of IL-1R on inflammation-induced hyperplasia was at the epithelial–stromal interaction rather than in reducing infection (Wang et al., 2015). The gene discussed is IL1R1; the disease is infection.