Indeed, when the tagged ctr4+ and ctr5+ alleles were co-expressed in ctr4Δ ctr5Δ cells, they functionally complemented the respiratory deficiency of the double mutant strain at the same level as the ctr4+ and ctr5+ wild-type, untagged alleles (Fig. 2 and data not shown). This evidence concerns the gene SLC6A8 and hyperinsulinemic hypoglycemia, familial, 4.