In breast cancer, TCGA analysisshowed that the SEMA6D-high patient group has decreased E-cadherin and increased SNAI2, ZEB1, and ZEB2, suggesting a correlationbetween SEMA6D and mesenchymal transition.15 In gastric cancer, colocalization of SEMA6D with SNAI1 protein (Snail)was positively correlated with invasion and lymph node metastasis.23 Here, we showed that SEMA6D regulated mRNA expressionof the EMT markers, mainly shifting toward a more mesenchymal patternin MCF10A cells. The gene discussed is SNAI1; the disease is gastric cancer.