Consistently, some research results showed that tumor cell-derived particles (membrane molecules, nuclear histones, caspases, microRNAs, and DNA) polarized TAMs into M2 phenotype and promoted the apoptosis of M1 TAMs, thus promoting tumor growth and metabolism, which were regulated by cGAS/STING/TBK1/STAT6 signal pathway (74). The gene discussed is TBK1; the disease is neoplasm.