Although a telomerase-independent alternative lengthening of telomeres (ALT) mechanism exists for telomere maintenance in cell lines and cancers in which telomerase is not active or is suppressed [237], [238], some studies suggest that ALT cells are not as biologically robust as telomerase-positive cancer cells, and may have heightened susceptibility to drug regimens that induce oxidative stress [239], [240]. The gene discussed is GPT; the disease is cancer.