The importance of the TAM regulatory mechanisms is evident in mice deficient for TAMs (Tyro3−/−, Axl−/−, Mer−/−), which have elevated levels of pro-inflammatory cytokines, including TNF-α and IL-6, and are prone to developing lymphoproliferative disorder and autoimmunity [6, 7]. The gene discussed is AXL; the disease is lymphoproliferative syndrome.