Similarly, in autoimmune diseases, such as rheumatoid arthritis and lupus, overactive JAK/STAT signaling can lead to excessive immune responses and tissue damage.315–318 Given its central role in disease pathophysiology, therapeutic strategies aimed at targeting components of the JAK/STAT pathway have emerged as promising approaches for managing these conditions. The gene discussed is SOAT1; the disease is systemic lupus erythematosus.