Consistent with our hypothesis, ATP11A was significantly increased during IPF in macrophages, a large proportion of which are derived from monocytes recruited to the lung during IPF,74 as well as in other airway epithelial cells and myofibroblasts, which are a key driver of fibrosis (Figure 9C; Table S6).65 During COVID-19, ATP11A was significantly decreased in AT1s, AT2s, other airway epithelial cells, concordant with the GWAS and eQTL data (Figure 9D; Table S7). The gene discussed is ATP11A; the disease is idiopathic pulmonary fibrosis.