Pitavastatin has also been shown to have an effect on inflammation and immune regulation, which may be due in part to a dose-dependent inhibition of monocyte proliferation through downregulation of the chemokine receptors CCR2 and CCR5 (Fujino et al. 2006), an effect mediated by inhibition of reactive oxygen species production induced by Rac-1, a rat sarcoma (Ras)-associated C3 botulinum toxin substrate 1 (Kaneyuki et al. 2007). This evidence concerns the gene CCR2 and sarcoma.