To further study the mechanism of KLF4 maintenance on stemness and mesenchymal phenotypes in CSCs, we knocked down and overexpressed KLF4 in cells and found that knockdown of KLF4 expression decreased stemness properties, along with decreased TGF‐β1, p‐Smad2/3 and up‐regulated Smad4.43, 44 Moreover, KLF4 knocking‐down effectively suppressed tumour cell migration and invasion capability, along with a decrease in expression of mesenchymal genes, such as Snail, a crucial downstream activator of TGF‐β1/Smad pathway.45 However, KLF4 overexpression also restored stemness and mesenchymal phenotypes. The gene discussed is SNAI1; the disease is neoplasm.