For example, astrocytes receive cGAMP from tumor cells through gap junctions and produce IFNα and tumor necrosis factor; as a result, these cytokines in turn enhance the survival and metastasis of the tumor cells.[67] In contrast, dendritic cells are primary immune responders to tumor‐derived cGAMP, which augments the antitumor functions of NK cells and T cells.[96, 97] Therefore, the bystander activation of STING pathway in surrounding cells elicits either pro‐ or antitumorigenic effects, depending on the cell type and context. The gene discussed is IFNA1; the disease is neoplasm.