Here, we have provided evidence that the use of aspirin and H‐151 in preventing cGAS and STING activity are efficient ways to inhibit senescent astrocyte‐driven inflammation in a relevant brain organoid model, and we have validated cGAS‐STING inhibition as a potent therapeutic target for A‐T neuropathology and potentially for other neurological diseases associated with premature ageing and significant self‐DNA‐induced SASP activation. The gene discussed is STING1; the disease is nervous system disorder.