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). This evidence concerns the gene TP63 and idiopathic pulmonary fibrosis.