The expression of GRP78 is highly relevant to apoptotic, immune, and fibrotic responses in the lung [75,76]; Grp78 heterozygosity (Grp78+/− mice were strongly protected from bleomycin-induced fibrosis and exhibited better lung function [75]; inactivation of GRP78 attenuated endothelial inflammation and permeability against acute lung injury [76], suggesting its possible involvement in lung pathology and function of COVID-19 patients. The gene discussed is HSPA5; the disease is COVID-19.