Similarly, our lab has recently synthesized and systematically validated high-affinity inhibitors of the glycolytic enzyme enolase and has drawn attention to the existence of subsets of cancers with homozygous deletions of ENO1, which are deficient in overall enolase activity and susceptible to inhibitors of oxidative phosphorylation by virtue of this glycolytic deficiency [9, 28]. The gene discussed is ENO1; the disease is cancer.