GCs constitute the cornerstone in the treatment of SLE, and its biological mechanism is regulated by the activation of GR.30 HSP90 is an important molecular chaperone and required for GR to bind the ligand and become active in vivo.9 However, Ouyang et al31 found that HSP90 expression in GC‐resistant patients was higher than that of in GC‐sensitive patients and that the increased HSP90 in GC‐resistant patients significantly tends to be intranuclear. Here, HSP90AA1 is linked to systemic lupus erythematosus.