This is attributed to TMAO’s ability to trigger TC ferroptosis through activation of the endoplasmic reticulum stress kinase PERK, thereby augmenting the in vivo anti-tumor immune response mediated by CD8+ T cells.135 These findings underscore the potential of microbial metabolites in enhancing treatment effectiveness by modulating the TME, presenting a promising avenue for novel therapeutic interventions. The gene discussed is CD8A; the disease is neoplasm.