In support of this therapeutic strategy, a recent report showed that crossing a Atp1a3 mouse model (Myskin) for Alternating Hemiplegia of Childhood (AHC) with a mouse model overexpressing a WT Atp1a3 allele could rescue the mutant phenotype through increased α3 pump activity (Kirshenbaum et al., 2016). This evidence concerns the gene ATP1A3 and alternating hemiplegia of childhood.