In vitro cellular models reminiscent of the in vivo PD pathology, however, indicated that the effects of VCE-003.2 to limit inflammation may be also exerted through additional mechanisms, including the possibility that VCE-003.2 targets PPARγ by acting through two binding sites at the LBP, one that is sensitive to T0070907 (canonical binding site) and other that is not affected by this PPARγ antagonist (alternative binding site). Here, PPARG is linked to Parkinson disease.