Therefore, DNA accumulated and activated STING.[47] However, mutant p53 interacted with TBK1 and destabilized the STING‐TBK1‐IRF3 complex, promoting immune evasion.[48] Moreover, different histone modifications such as epigenetic suppression of STING via the histone H3K4 lysine demethylase KDM5 in breast cancer cells[49] or a STING promoter hypermethylation silencing STING expression[50] are utilized by the cancer cells to repress STING. The gene discussed is STING1; the disease is breast carcinoma.