Moreover, the increased TLR4 expression was mainly localized within Iba1-positive microglia (Fig. 1d), suggesting that an increase in microglial TLR4 might be crucial for the pathogenesis of PD, and the discovery of endogenous molecules involved in the induction of microglial TLR4 might be useful for guiding the development of knowledge-based targeted therapeutics for PD. Here, AIF1 is linked to Parkinson disease.