In in vitro studies, TLR4 disclose to communicate with alpha‐synuclein, activating the response of microglia namely alpha‐synuclein uptake, proinflammatory cytokine release and oxidative stress stimulation and these findings were supported by a 1‐methyl‐4‐phenyl‐1,2,3,6 tetrahydropyridin (MPTP) induced murine prototype of PD where the genetic nonappearance of TLR4 signaling safeguarded the mice from neurodegeneration disclosing the chief function of TLR4 in the development of PD.14 This evidence concerns the gene TLR4 and Parkinson disease.