Based on this mechanistic link between efferocytosis and TGβ production, we hypothesized that persistent alveolar epithelial cell apoptosis, as occurs in lung fibrosis, might lead to protracted TGFβ expression as a result of ongoing ingestion of apoptotic cells by alveolar macrophages and that this macrophage response might translate into fibrosis rather than tissue homeostasis. This evidence concerns the gene TGFB1 and pulmonary fibrosis.