In IPF, fibroblasts exhibit unregulated proliferation, migration, and differentiation into myofibroblasts which overproduce ECM components.[29, 30] We further established that P61‐Sema3E is the predominantly active form that promotes lung fibrosis, as evidenced by stimulating fibroblasts with recombinant proteins of different Sema3E forms. Here, SEMA3E is linked to pulmonary fibrosis.