Moreover, recent research has reported some evidence of a relationship between PD pathogenesis in humans and dysfunctional HCN channels by analyzing electrophysiological data obtained from models treated with the toxic chemical 1-methyl-4-phenylpyridinium (MPP+), which can induce PD-like selective degeneration of nigral dopaminergic neurons, suggesting that HCN blockage from MPP+ treatment may increase synaptic excitability (Masi et al., 2013). The gene discussed is MALAT1; the disease is Parkinson disease.