Given that JAK/STAT plays a crucial role in the pathological progression of inflammatory arthritis and that JAK inhibitors have been successfully translated into clinical use for treating autoimmune diseases, including several types of inflammatory arthritis [50–52], we hypothesize that the overexpression of Pim2 in inflammatory arthritis may be due to aberrant activation of the JAK/STAT signaling pathway. Here, SOAT1 is linked to autoimmune disease.