Indicating that cGAS recruitment to micronuclei and subsequent STING activation is due to cytosolic exposure of micronuclei DNA, overexpression of LaminB2 (LMNB2) in cancer cell lines, shown to prevent this process17, inhibited cGAS micronuclear localization following treatment (without influencing micronuclei formation per se) and prevented STAT1 and NF-κB activation (Fig. 1c, e). The gene discussed is STING1; the disease is cancer.