NTRK1 and COVID-19: sMERTK can be produced by proteolytic ectodomain shedding of membrane-bound (mb) MERTK, a member of the Tyro-Axl-MerTK (TAM) family of receptor tyrosine kinases, the activation of which leads to immunosuppression and macrophage-mediated apoptotic cell phagocytosis.61, 62, 63,85 sMERTK can act as a competitive inhibitor of MERTK signaling by sequestering ligands that could otherwise bind to mbMERTK.61, 62, 63 In the context of COVID-19, impaired MERTK signaling has been proposed as a link between the hyperinflammatory and hypercoagulative state observed in patients with severe disease.61