Traditionally, G6PD studies have been focused on human red cells. G6PD in nucleated cells regulates cellular processes, including cell proliferation, cell death, autophagy, inflammation, and tumorigenesis. G6PD deficiency reduces replicative potential in human fibroblasts, leading to early-onset senescence [27]. Such premature senescence is most likely due to elevated oxidative stress rather than increased telomere shortening. Approaches using biochemical inhibitors or RNAi knockdown against G6PD in several cell lines demonstrate that decreased G6PD activity is associated with growth retardation [28]. The most common form of cell death caused by G6PD activity suppression is apoptosis.