SEMA3E and idiopathic pulmonary fibrosis: 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.