Preclinical studies have demonstrated that A. muciniphila and its derivatives exert protective effects across multiple disease models—for example, the tripeptide RKH mitigates lethal sepsis by blocking TLR4 signaling, and A. muciniphila-based interventions promote neurorepair via modulation of the gut–brain axis—thus supporting its translational potential while remaining at the preclinical stage of development [58,59]. The gene discussed is TLR4; the disease is Sepsis.