PPARG and gout: These studies also showed that signaling pathways (p38, NFκB, ERK1/2) activated via TLR2 and TL4 were inhibited by PPARγ in various condition, such as in T2D, cardiomyopathy, or in MSU crystal-induced acute inflammation in gout, aiding in the resolution of the inflammatory response (191–195) (Figure 5).