If validated with wild-type strains isolated from immunotherapy-responsive patients, we anticipate two potential outcomes: (1) strain-specific variations in propionate production or immunomodulatory molecules may further amplify CD8+ T cell infiltration through the synergistic engagement of the Meox1-Cxcr6/Ccl5 axis; (2) host-microbe co-evolutionary adaptations might enhance bacterial persistence in irradiated tumour microenvironments, sustaining H3K14 acetylation-mediated epigenetic reprogramming. The gene discussed is CCL5; the disease is neoplasm.