Therapeutic targeting of JAK-STAT components with inhibitors (e.g., tofacitinib, ruxolitinib) can disrupt this vicious cycle by blocking downstream phosphorylation and nuclear translocation of STATs, thereby reducing cytokine production and immune cell activation, as evidenced in preclinical and clinical studies of sarcoidosis and granuloma annulare. The gene discussed is SOAT1; the disease is granuloma annulare.