In vivo studies in mouse models have also contributed to our understanding of the physiological functions of mammalian P4-ATPases: Atp8a1-deficient mice exhibit delayed hippocampus-dependent learning, Atp8a2-mutant mice display neurological abnormalities such as ataxia derived from axonal degeneration and loss of visual/auditory functions, and Atp11c-mutant mice show arrested B cell development17, 21. This evidence concerns the gene ATP8A2 and cerebellar ataxia.