Oncogenic RAS signaling leads to mitochondrial dysfunction, resulting in increased mitochondrial production of reactive oxygen species (ROS), which contributes to cellular senescence (Moiseeva et al. 2009). The exact biochemical mechanism of RAS-induced mitochondrial dysfunction has not been established. Prolonged exposure to interferon-beta (INFB, INF-beta) also results in increased ROS concentration in the cell and triggers cellular senescence (Moiseeva et al. 2006). Although the positive regulation of ROS production by interferon signaling is well documented (Huang et al. 2007, Yang et al. 2007, Yim et al. 2012), the precise mechanism is not known.