Baicalin still decreased CX3CR1 expression by 62%, phosphorylated AKT levels by 48%, and the lung wet-to-dry weight ratio by 28% in CX3CL1-knockout mice, confirming the role of CX3CL1 in mediating LPS-induced ALI pathology and indicating that baicalin’s protective effects are at least partially dependent on the CX3CL1-CX3CR1 axis [117]. The gene discussed is CX3CL1; the disease is acute respiratory distress syndrome.