Because SCN2A variant classification does not always align perfectly with SRD patient phenotypes, this review synthesizes the existing literature beyond the lens of GOF and LOF distinction by first reviewing our current understanding of the cellular functions of Nav1.2 to generate a foundation with which to contextualize the non‐human mammalian models of SRDs presented later. Here, SCN2A is linked to dopa-responsive dystonia due to sepiapterin reductase deficiency.