Female mice with a deletion of the RANK gene in neurons and astrocytes exhibit elevated baseline body temperatures.[181, 183] During the acute phase, RANKL and RANK mRNA levels increase and are expressed in activated microglia and macrophages.[184] RANKL/RANK signaling can mitigate inflammation through the Toll‐like receptor signaling pathway in microglia.[177] Thus, the OPG/RANKL/RANK axis holds promising potential for the treatment of ischemic brain inflammation. The gene discussed is TNFSF11; the disease is brain inflammatory disease.