For example, mROS can reach extra-mitochondrial redox-sensitive targets like transcription factors [HIF1α, p53, or nuclear factor of activated T cells (NFAT); Wang et al., 1995, 2000; Huang et al., 1996, 2000; Xie et al., 2001; Bonnet et al., 2007a] and Kv channels in the plasma membrane (Weir et al., 2005; Bonnet et al., 2007a), further facilitating apoptosis and decreasing the proliferative potential of cancer cells, as we discuss below. The gene discussed is HIF1A; the disease is cancer.