This receptor plays a critical role in regulating intracellular calcium levels (Mangla et al., 2020), and, as calcium signaling is directly linked to ER homeostasis and eIF2α signaling, it is reasonable to speculate that the combination of calcium signaling dysregulation and Prkralear-5J mutation may result in the enhanced dystonia phenotype, especially because we have previously linked PACT/RAX-mediated PKR regulation with a central role in cellular fate in response to ER stress (Singh et al., 2009; Vaughn et al., 2015; Burnett et al., 2019). Here, RAX is linked to Dystonia.