Trpm3-EGFP-CreERT2 mice are generated via genome editing by replacing the TAA stop codon of the mouse Trpm3 gene with a P2A-EGFP-T2A-CreERT2 cassette, enabling co-expression of CreERT2 recombinase and EGFP driven by endogenous Trpm3 regulatory elements. The 2A peptide linkage overcomes reduced protein activity and downstream gene expression typically associated with multi-gene constructs. 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, tamoxifen induction triggers Cre recombinase-mediated sequence recombination between loxP sites in Trpm3-positive cells of offspring. Beyond Cre-loxP gene recombination, this model enables EGFP-based fluorescent tracing.