Together with other reports suggesting that mutant HTT proteins modulate N-type voltage-gated Ca2+ channels through their interaction with N-type voltage-gated Ca2+ channels and their binding proteins (Miller et al., 2003; Swayne et al., 2005; Silva et al., 2017), our results suggest that N-type voltage-gated Ca2+ channels, play an important role in the increased presynaptic Ca2+ influx and synaptic vesicle release in cortical neurons from HD mice. The gene discussed is HTT; the disease is Huntington disease.