Hypercholesterolemia is a major contributor to the risk of developing a range of severe health conditions, including cardiovascular diseases (CVDs), brain diseases, nephropathy, retinopathy, and neuropathy. The primary function of statins is to mitigate cholesterol content via suppressing 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA-R). This study aims to evaluate the anti-inflammatory mechanisms underlying the cholesterol-reducing capabilities of statins. The effects of statins beyond their cholesterol-lowering action are referred to as pleiotropic effects. Anti-inflammatory effects are among the pleiotropic roles of statins. These effects include lowering triglyceride (TG) concentrations, elevating high-density lipoprotein cholesterol (HDL-C) and interleukin 10 (IL-10), and downregulating inflammatory markers. Part of the anti-inflammatory effects results from the suppression of the activity of the Rho and Ras protein families, thus inhibiting nuclear factor kappa-light-chain enhancer of activated B cells (NF-κB) and activating protein-1 (AP-1). In recent years, the anti-inflammatory effects of atorvastatin, simvastatin, and rosuvastatin have been studied more extensively than those of other statins. In fact, these statins are more prominent.