Future studies on L155P outside the scope of this case study will include an examination of its behavior in heteromeric complexes with KCNA2 and KCNA4, with which KCNA1 is thought to co-assemble in vivo in addition to forming homomeric KCNA1 channels as it is possible this may give some clues to why some KCNA1 mutants cause expanded phenotypes in addition to episodic ataxia (17–19). This evidence concerns the gene KCNA4 and Familial paroxysmal ataxia.