By contrast, our SMC-specific Prdm16 KO models did not show increased expression of Adam12 or inflammatory markers such as Cd68 and Lgals3. However, PRDM16 did downregulate expression of tumor necrosis factor receptor superfamily gene Tnfrsf11b. In atherosclerosis, TNFRSF11b is involved in ECM remodeling and repression of vascular calcification, rather than driving inflammation32,44. This evidence concerns the gene ADAM12 and atherosclerosis.