Monocytes also promote fibrosis formation through two critical mechanisms: one is to produce proinflammatory cytokines [IFN-α, MIB-α (CCL3) and MIP-1β (CCL4)] to promote myofibroblast differentiation, and the other way is to serve as progenitor fibrocytes to induce pulmonary fibrosis (27). This evidence concerns the gene CCL3 and pulmonary fibrosis.