While CD36 has been previously implicated in pro-inflammatory responses, particularly in foam cell formation and atherosclerosis via TLR2 signaling,6,7 our findings in Pg-LPS-stimulated macrophages reveal a contrasting role: CD36 expression was upregulated following fenofibrate treatment and was associated with enhanced IL-10 production, reduced NF-κB activation, and increased expression of M2 surface markers. The gene discussed is TLR2; the disease is atherosclerosis.