Strong evidence links these two proteins with altered neuronal communication and deficient long-term depression induction in the corticostriatal circuitry of HD (Baydyuk et al., 2011; Besusso et al., 2013; Kim et al., 2020) Thus, defining the role of VPS13A in striatal synaptic plasticity and MSN communication may constitute a key point to understanding the specific striatal vulnerability not only in ChAc, but also in HD. This evidence concerns the gene VPS13A and Huntington disease.