In this regard, our data showing that IM entry uses an ACE2-independent mechanism that relies on CD209 and a region of the viral Spike protein outside the canonical ACE2 interface may explain why therapeutic antibodies have failed in severe cases of COVID-19 lung inflammation—they block viral entry into airway and alveolar epithelial cells that initiate the disease, but not into the IMs that we propose catalyze the inflammatory and fibrotic phase (Fig. 6 e). The gene discussed is CD209; the disease is COVID-19.