RAC1 and Sepsis: Mechanistic studies reveal that rhamnose directly binds to and activates solute carrier family 12 member 4 (SLC12A4) on macrophages, triggering the Ras-related C3 botulinum toxin substrate 1 (Rac1)/cell division cycle 42 homolog (Cdc42) signaling axis to enhance phagocytic activity and reduce sepsis-induced organ damage and mortality [47]).