According to our previous experimental data, EMT is a consequence of external stimuli from the tumor microenvironment, such as transforming-growth-factor-beta-1 (TGF-beta1) or Interleukin 6 (IL-6) [5], cellular metabolic stress and internal cell-events [1,6], which activate EMT-associated transcription factors as the members of SNAI gene family. The gene discussed is IL6; the disease is neoplasm.