In line with this, our in‐depth analysis revealed that RA‐induced NF‐κB and type I IFN activation in tumor cells depended on the cGAS/STING as silence of cGAS or STING, but not RIG‐1, MDA‐5, or TLR3, abolished NF‐κB and type I IFN activation. Here, CGAS is linked to neoplasm.