A TKTL1-based lactobacillae-like glucose degradation pathway has been postulated to explain the observed glucose metabolism in tumours (Coy et al, 2005), and such a pathway would result in enhanced glucose usage, enhanced carbonic anhydrase enzyme activity, enhanced de novo fatty acid synthesis, inhibition of Embden-Meyerhof glycolysis, enhanced lactate production, and mitochondria-independent ATP generation. Here, TKTL1 is linked to neoplasm.