In contrast, addition of NPY to the AKI mice and LPS-stimulated BMDMs was capable of dose-dependently upregulating Y1R signaling, thereby blocking NF-κB-Mincle-mediated M1 macrophage activation and proinflammatory cytokines including IL-1β, TNFα, IL-6, and MCP-1, which was reversed by silencing NPY in LPS-stimulated BMDMs. The gene discussed is IL1B; the disease is acute kidney injury.