The most upstream pro-inflammatory effector in atherosclerosis is NF-kB [117], and the presence of PGC-1α can decrease the activity of NF-kB and tumor necrosis factor α (TNFα), consequently blocking oxLDL-related inflammation, regulating vascular endothelial growth factor-1 (VEGF1) expression, and stimulating angiogenesis [107]. This evidence concerns the gene PPARGC1A and atherosclerosis.