In SLE, elevated levels of IFN-γ have been associated with disease activity and severity, contributing to the pathogenesis of SLE through the IFNGR1/2-pSTAT1-TBX21 signaling axis, promoting Th1 cell differentiation and activation, as well as B-cell complex formation, thereby exacerbating autoimmune responses [141]. Here, IFNG is linked to systemic lupus erythematosus.