For instance, mechanisms that promote hyperpolarization of thalamic relay neurons and cause T-type Ca2+ channel spikes (i.e., the Dgcr8–miR-338-3p–Drd2 mechanism in 22q11DS or CaV3.3-dependent TRN inhibition) may synergistically produce sufficient hyperpolarization to activate T-type Ca2+ channels, which in turn would cause the channels to produce abnormal delta-frequency oscillations (Richard et al., 2017). Here, DGCR8 is linked to 22q11.2 deletion syndrome.