Considering the ubiquitous expression of Cav3.2 VGCCs and the structural similarities among T-type Ca2+ channels, the design of astrocyte-selective agonists or the indirect targeting of the ubiquitinases and de-ubiquitinases that regulate the turnover of Cav3.2 channels could represent new neuroprotective approaches for synucleinopathies. The gene discussed is CACNA1H; the disease is synucleinopathy.