With those evident clinical similarities and knowing that gain-of-function CACNA1A mutations can lead to both paroxysmal neurological symptoms and cerebellar symptoms including cerebellar atrophy (such as progressive or congenital ataxia) [19], we explore the hypothesis of increased CaV2.1 activity due to deficient N-glycosylation as an underlying biological reason, offering a potential novel pathomechanism of SLE and cerebellar syndrome in PMM2-CDG. Here, CACNA1A is linked to Cerebellar atrophy.