The K10Cx26 (D66H), Cre;Cx26+/floxS17F, Cx26-G45E, and pgk-Cre;Cx30+/floxA88V mice all show obvious epidermal hyperkeratosis, while homozygous loss of Cx26 or Cx30 (in humans or mice) results in no clinically discernible epidermal abnormality [44,50,51,88,172,173,174]. This evidence concerns the gene PRKG1 and Hyperkeratosis.