CLDN18 and neoplasm: As shown in Fig. 1k, l, we found that in the Cldn18-CreERT2; Apcfl/fl; Trp53fl/fl; KrasG12D (a.k.a. Cldn18-ATK) mice, which were generated by specifically knocking out APC and Trp53, and expressing KrasG12D in the gastric epithelium using a Cre recombinase under the Cldn18 promoter25, the CAD levels in hyperplastic gastric tumor tissues were significantly reduced after the treatment with 5-FU, resulting in a significant reduction in tumor size.