Furthermore, the CD146/Gp130 signaling axis also played a positive role in JNK activation (Figure 7D), which has been reported to positively regulate the SOCS3 expression.[33] Collectively, our findings suggest that CD146‐Gp130 interaction contributes to the pro‐inflammatory polarization of macrophages under hyperlipidemia conditions and that polarization is regulated by the balance between STAT3 and JNK signaling (Figure 7E, proposed model). This evidence concerns the gene STAT3 and hyperlipidemia.