Jarid1b represents a barrier to ESC EMT and the reprogramming of differentiated cells by regulating mesenchymal master regulators,32 whereas in human lung and colon cancer cells, overexpression of Jarid1b promotes the EMT process via upregulating the expression of Zeb1 and Zeb2, which are targeted by microRNA‐200.33 Our results showed that Jarid1b overexpression impaired cell migration in a wound healing assay and promoted the expression of MET genes, among which Ovol1 has been proven to be a key molecule in epithelial differentiation. The gene discussed is KDM5B; the disease is colonic neoplasm.