SREBP2 and LXR pathways regulating inflammation. Upregulation of cholesterol synthesis by SREBP2 also involves NLRP3 activation as SCAP forms a ternary complex and escorts both proteins to the Golgi apparatus (1). NLRP3 and inflammasome activation leads to IL-1β release. Increased cholesterol synthesis induces mitochondrial damage, release of mitochondrial DNA, and activation of the AIM2 component of the inflammasome (2). Oxysterols, such as 25-HC, inhibit inflammation by blocking cholesterol synthesis and inflammasome activation and activating LXRs through multiple mechanisms (3). Inflammasome activation is blocked by inhibition of cholesterol synthesis and avoidance of SCAP/SREBP2 and NLRP3 translocation to the Golgi apparatus. Cholesterol synthesis also leads to formation of GGPP and FPP isoprenoids, which induce prenylation and activation of RhoA, Ras, Rac, Cdc42, and Rab5 small GTPases, which are involved in inflammasome activation, antigen presentation, and cell movement (4). FPP, farnesyl pyrophosphate; GGPP, geranylgeranyl pyrophosphate.