By using a bovine endometrial epithelial cell inflammation model and a mouse lipopolysaccharide-mediated endometritis model, the author confirmed that miR-34a/miR-193a-3p was upregulated by IL-1β and suppressed the level of the LGR4 3′UTR, which in turn amplified the inflammatory response through activating the phosphorylation of NF-κB p65 pathway, suggesting miR-34a/miR-193a-3p-LGR4 playing a pivotal role in endometritis (Ma et al., 2021; Yin et al., 2021). The gene discussed is LGR4; the disease is endometritis.