Multiple studies using a TMPD‐induced SLE mouse model have demonstrated the critical role of cGAS–STING signaling in lupus pathogenesis.[29, 49] Our findings showed that Pbld‐deficiency in Pristane‐induced lupus (PIL) mice resulted in diminished autoimmune phenotypes and responses, including attenuated pathological damage, downregulated STING expression, and decreased type I IFN production compared with those in WT mice. The gene discussed is CGAS; the disease is hyperinsulinemic hypoglycemia, familial, 4.