CDKN2A is a negative regulator of BCR stimulation-induced cell cycle.[37] Senescence, a state of irreversible cell cycle arrest, may be caused by mitochondrial dysfunction.[38,39] Mitochondrial dysfunction has been found to play an important role in the pathogenesis of IPF and fibrosis in animal models.[40,41] The pathological mechanism of cuproptosis includes disruption of mitochondrial metabolic enzymes.[42] Therefore, we conclude that CDKN2A may influence pulmonary fibrosis and molecular subtypes by affecting mitochondrial function. Here, BCR is linked to pulmonary fibrosis.