Several previous studies using Mertk KO mouse models have shown strong phenotypes for loss-of-function Mertk, including an (i) enhanced susceptibility to endotoxin [59], (ii) failed efferocytosis and polarization of macrophages [13], (iii) susceptibility to chronic inflammation and SLE-like autoimmunity [11,15], and (iv) an auto-antibody production and rheumatoid arthritis [60,61]. The gene discussed is MERTK; the disease is rheumatoid arthritis.