To do so, we generated mice with a fibroblast-specific conditional deletion of KLF4 [Col1α2-Cre-ER(T)+/0-KLF4fl/fl or cKLF4 KO] by crossing floxed KLF4 mice (KLF4fl/fl) with mice expressing Cre under a Col1a2 promoter [Col1α2-Cre-ER(T)+/0] and subjected them to the commonly used single-dose bleomycin-induced model of pulmonary fibrosis. Here, COL1A2 is linked to pulmonary fibrosis.