However, as this repression is reciprocal, i.e. SNAI2 itself represses KLF4 as well, a balance between both factors can determine a transit towards a mesenchymal state, with a positive feedback on expression of the central TGFß components, mediated by KLF4. Similarly, the extensively described tumor suppressor KLF6 antagonizes EMT, but activates transcription of TGFß ligand and receptors 1 and 2 [66]. Here, KLF6 is linked to neoplasm.