Importantly, accumulating evidence has shifted this perspective, suggesting IPF as predominantly an epithelial‐driven condition.[10, 11, 12, 13, 14] Recurrent and unresolved epithelial injury leads to aberrant activation of basal cells, marked by KRT5+/KRT17+/COL1A1+, promoting the pro‐fibrotic cell fates and bronchiolization process in the diseased lung.[15, 16] However, the underlying mechanisms shaping this disease phenotype and the fibrotic cell fate of lung epithelial progenitors/stem cells remain poorly understood, highlighting a critical gap in current IPF research.[17, 18]. The gene discussed is COL1A1; the disease is idiopathic pulmonary fibrosis.