The excessive production of proinflammatory cytokines can disrupt immune homeostasis, leading to autoimmune diseases such as rheumatoid arthritis (RA) and SLE, with TNF‐α and IL‐6 being prime targets for drug development.[33] While clinical applications of monoclonal antibodies targeting these cytokines or their receptors have been successful, concerns about side effects drive the search for new therapeutic targets and strategies.[5, 34] Our findings highlight the pivotal role of HDAC7 in mediating LPS‐induced inflammatory responses by activating downstream MAPK/NF‐κB pathways. This evidence concerns the gene NFKB1 and systemic lupus erythematosus.