While previous studies have shown rifaximin’s anti-fibrotic effects [36–41] and others have demonstrated the importance of LSECs in liver fibrosis [17], this work uniquely connects these two areas through a mechanistic pathway involving LPS-TLR4-eNOS axis, advancing our mechanistic understanding of the gut-liver axis by providing a pathway linking gut dysbiosis to LSEC dysfunction. Here, TLR4 is linked to Hepatic fibrosis.