STING‐signaling in immune cells promotes type I IFN‐dependent spontaneous T‐cell priming that increases tumor immunogenicity and improves cancer immunotherapy.[31] To investigate whether NAMPT‐deficient TAMs improved T‐cell function, activated splenocytes were cultured with TAMs (generated via co‐culture with dying cancer cells). This evidence concerns the gene STING1 and neoplasm.