In this study, we speculated and obtained clues that KAT2A might promote the inflammation amplification of SLE via regulation on cGAS: [1] the upregulated KAT2A co-localizes with cGAS in PBMCs and positively related with cGAS and disease activity in SLE; [2] KAT2A inhibition down-regulated cGAS, STING at mRNA level, as well as IFN-I expression in SLE. The gene discussed is STING1; the disease is systemic lupus erythematosus.