Increased lung fibrosis evident by increased deposition of collagen in the absence of Sema3E which was reversed upon Sem3E treatment could be attributed to an unknown mechanism in which Sema3E functions as an anti-fibrotic mediator probably via reduction of migration and proliferation of fibroblasts as the main source of collagen production [23]. The gene discussed is SEMA3E; the disease is pulmonary fibrosis.