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are cell\u2013cell adhesion molecules, fundamental for cell architecture and polarity. E-cadherin to P-cadherin switch can rescue adherens junctions in epithelial tumours. Herein, we disclose a mechanism for E-cadherin to P-cadherin switch in gastric cancers. CDH1 and CDH3 mRNA expression was obtained from 42 gastric tumours\u2019 RNA-seq data. CRISPR-Cas9 was used to knock out CDH1 and a putative regulatory element. CDH1-depleted and parental cells were submitted to proteomics and enrichment GO terms analysis; ATAC-seq\/4C-seq with a CDH1 promoter viewpoint to assess chromatin accessibility and conformation; and RT-PCR\/flow cytometry to assess CDH1\/E-cadherin and CDH3\/P-cadherin expression. In 42% of gastric tumours analysed, CDH1 to CDH3 switch was observed. CDH1 knockout triggered CDH1\/E-cadherin complete loss and CDH3\/P-cadherin expression increase at plasma membrane. This switch, likely rescuing adherens junctions, increased cell migration\/proliferation, commonly observed in aggressive tumours. E- to P-cadherin switch accompanied increased CDH1 promoter interactions with CDH3\u2013eQTL, absent in normal stomach and parental cells. CDH3\u2013eQTL deletion promotes CDH3\/CDH1 reduced expression. These data provide evidence that loss of CDH1\/E-cadherin expression alters the CDH3 locus chromatin conformation, allowing a CDH1 promoter interaction with a CDH3-eQTL, and promoting CDH3\/P-cadherin expression. 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