The SOX2−/TP63+ Wnt-activated transcriptional signature of KRT5−/KRT17+ basaloid cells in IPF and SOX2− signature of KRT5−/KRT17+ basaloid cells in post-COVID-19 fibrosis suggest that loss of SOX2 expression may explain the formation of these distinct dysplastic lesions in lung disease (Fig. 7b). The gene discussed is KRT17; the disease is COVID-19.