NFKB1 and atherosclerosis: To further explore the potential mechanisms by which H2S inhibits OX-LDL induced the inflammatory response in atherosclerosis, the scientists from Peking University revealed that endogenous H2S inhibited ox-LDL-induced macrophage inflammation by suppressing NF-κB p65 phosphorylation, nuclear translocation, DNA binding activity, and recruitment to the MCP-1 promoter.