However, unlike the above cancer cell lines and Myc−/− rat fibroblasts, which cannot sustain adequate ATP levels, an ∼2-fold increase in mitochondrial mass observed in MycKO MEFs was postulated to represent a means of compensating for energy generating defects as often occurs in association with aging, senescence and various mitochondrial stresses and diseases (Trifunovic et al., 2004; Barrientos, 2012; Miwa et al., 2022). The gene discussed is MYC; the disease is cancer.