In bleomycin models of pulmonary fibrosis, epithelial cell subpopulations enriched in expression of Krt8, Cldn4, Lgals3, and Krt19, which have been referred to as pre-alveolar type 1 transitional cell state, damage-association transition progenitors, and Krt8+ alveolar differentiation intermediates, appear to emerge from incomplete differentiation of AT2 cells (16–18). This evidence concerns the gene CLDN4 and pulmonary fibrosis.