The underlying cause remains elusive, and it is unknown whether this is a mouse-specific progression or reflects processes that may also be involved in human HI, although the correlative data is substantial.36 In demonstrating a similar glucose-intolerant and non-hypoglycemic phenotype in zebrafish that completely lacks KATP channels, these SUR1−/− fish thus confirm a common finding from fish to mouse and may provide a useful model for further exploring the unexplained phenomenon of glucose intolerance and even diabetes in KATP-dependent HI patients. This evidence concerns the gene ABCC8 and Glucose intolerance.