This conclusion was based on a number of criteria, including injecting the same concentrations of Cx26 and Cx30 cRNA, observing high expression of Cx30 with fluorescent tagging despite showing low levels of functional hemichannel currents, observing high levels of Cx30-mediated GJ currents under the same conditions, and showing that Cx30 contributed to the expression of large, Ca2+-sensitive hemichannel currents when co-expressed with Cx26(D50N/A), KID syndrome mutants in which position 50 is neutralized. This evidence concerns the gene GJB2 and KID syndrome.