Contrastingly, the renal tissue of GWI mice co-exposed with antibiotic treatment for 20 weeks showed a significantly increased deposition of fibronectin and increased α-SMA immunoreactivity, indicating that the exposure to prolonged antibiotic exposure aggravates renal pathology induced by GW chemicals, further aiding in the development of renal fibrosis-like pathology, possibly via TGF-β-mediated miR-21/PTEN/AKT signaling. The gene discussed is TGFB1; the disease is renal fibrosis.