These data supported the conclusion that the toxicity of the acute treatment with TGFβ, detected both by viability assay and by LDH release, associated with the decrease in mitochondrial potential, was due to the increased ROS production, whereas the prolonged TGFβ treatment at low doses did not damage the human pancreatic cancer cells because ROS levels did not change. The gene discussed is TGFB1; the disease is pancreatic neoplasm.