We previously showed that angiopoietin-like protein (Angptl)2, a mediator of chronic inflammation, is highly expressed in LF tissues of patients with LSCS and is induced in LF fibroblasts by mechanical stress; furthermore, Angptl2 stimulates transforming growth factor -β1 expression, leading to LF fibrosis, and interleukin (IL)-6 expression [10, 11]. This evidence concerns the gene ANGPTL2 and Lassa fever.