Upon activation by cytokines such as IL-33 which is released from injured AECs, macrophages can produce multiple pro-inflammatory cytokines and chemokines such as tumor necrosis factor α (TNF-α), IL-1β, C-C motif ligand 2 (CCL2) and CCL12, which initiate inflammation and induce myofibroblast activation, thereby contributing to lung fibrosis [6, 7]. The gene discussed is IL33; the disease is pulmonary fibrosis.