Indeed, Seo Jaesung et al. had shown that the suppression of GPR177 (Wntless, WLS), an essential protein for the secretion of Wnt, suppressed tumor gastric proliferation [51]; while Suzuki et al., by using a specific model of stomach with a claudin-18.2 deficiency junction (stCldn18-KO) that reproduced the cancer Correa cascade in the absence of H. pylori infection, demonstrated that Wnt1 overexpression produced gastric tumors faster than stCldn18-KO without Wnt1 [52]. This evidence concerns the gene WLS and gastric neoplasm.