Krt13-CreERT2 mice are generated via genome editing by replacing the TAA stop codon of the mouse Krt13 gene with a P2A-CreERT2 cassette. Without tamoxifen treatment, CreERT2 recombinase primarily resides in the cytoplasm; nuclear translocation and recombination activity of CreERT2 only occur upon tamoxifen stimulation. When crossed with mice containing loxP sites, offspring are expected to undergo Cre-mediated recombination between loxP sites specifically in Krt13-positive cells following tamoxifen administration.