A bifunctional HDAC and PARP inhibitor (hereafter referred to as P2) upregulated STING expression in pancreatic cancer cells, accompanied by cytosolic DNA accumulation and activation of the tumor‐intrinsic cGAS–STING pathway, as evidenced by increased phosphorylation of TANK‐binding kinase 1 (TBK1) and elevated production of type I and III IFNs. The gene discussed is STING1; the disease is pancreatic neoplasm.