Consistent with a role in metabolic reprogramming, as commonly observed in cancer, a significant body of published evidence indicates that GLO1 expression plays an essential role in maintaining high glycolytic flux (as it occurs in tumors in the context of aerobic glycolysis, commonly referred to as ‘the Warburg effect’), enabling escape from apoptosis, and also facilitating tumorigenic adaptations to hypoxia [5,6]. The gene discussed is GLO1; the disease is cancer.