In mouse models of lung fibrosis and precision-cut lung slices from IPF patient ex vivo, selective removal of p16-expressing senescent fibroblasts or senolytic treatments attenuate fibrotic phenotype, suggesting that senescent fibroblasts participate in key aspects of lung fibrosis (Cooley et al., 2023; Lee et al., 2024). Here, CDKN2A is linked to pulmonary fibrosis.