Consistent with this, we have recently shown that AT1-AAs induced neurodegeneration in PD models through several mechanisms, such as promoting oxidative stress and neuroinflammation, intraneuronal calcium raising, alpha-synuclein aggregation, and blood–brain barrier disruption, which were mitigated by treatment with AT1 receptor blockers [13,14,19]. The gene discussed is SNCA; the disease is Parkinson disease.