To determine whether this mechanism is widespread across different types of cancer, we first evaluated the nuclear accumulation of pSMAD2 and pSMAD3 in fibrosarcoma (HT-1080), breast adenocarcinoma (MDA-MB-231) and lung carcinoma (A549) cells incubated under normoxic (21% O2), hypoxic (1% O2) or TGFβ1-supplemented conditions. The gene discussed is TGFB1; the disease is cancer.