While protective against excessive inflammation physiologically,[101] elevated tumor IL‐10 inhibits dendritic cell maturation (via downregulation of MHC‐II, CD80, CD86), impairing T cell activation and compromising antitumor efficacy.[9, 20, 102] Precise dose control is also complicated by the bacteria's living, proliferative nature.[9] Furthermore, host microbial ecology and immunological memory can cause inconsistent outcomes through competition with commensals.[103] Long‐term safety concerns include risks of systemic infection, chronic inflammation, and excessive immune activation.[9, 104]. The gene discussed is CD86; the disease is neoplasm.