Very recently, in a 5XFAD transgenic mouse model of AD, chronic administration of biased and selective β1 adrenergic receptor agonist, xamoterol, reduced Aβ toxicity-associated neuroinflammation and tau by reducing microgliosis and astrogliosis markers, allograft inflammatory factor 1 (Iba1) and glial fibrillary acidic protein (GFAP), as well as inflammatory markers, Iba1, CD74, CD14 and TGFβ. The gene discussed is CD74; the disease is Alzheimer disease.