Carta et al. (2011) demonstrated that rosiglitazone was able to modulate PPARγ receptor expression specifically in microglia without impacting neuronal receptor levels to attenuate neuroinflammation and degeneration in a model of Parkinson’s disease. Further work suggests that the anti-inflammatory action may be through suppression of TNFα (Carta et al., 2011; Liu et al., 2016) or possibly due to rosiglitazone’s ability to drive a microglial switch from a neuroinflammatory activation state to a neuroprotective activation state (Subramaniam and Federoff, 2017; Ji et al., 2018). Here, TNF is linked to Parkinson disease.