A previous study reported that the cGAS‐STING pathway activates the canonical/non‐canonical NF‐κB and STAT3 pathways to promote tumor cell proliferation.[23] G150‐treated PTCL cells showed decreased p‐STAT3 and p‐RELB expression compared to the negative control (Figure 3G,H; Figure S3F,G, Supporting Information). The gene discussed is CGAS; the disease is mature T-cell and NK-cell non-Hodgkin lymphoma.