Combined with the reduced expression of the glucose transporter Slc2a1/Glut1, the key determinant of glucose uptake and transcripts for 6Pgd, the rate-limiting step in the pentose phosphate pathway (Fig 2H and 2I), these findings collectively suggest that a major effect of HFDs on tumor growth may occur via the down-regulation of glucose uptake and the shunting of its immediate metabolite, glucose-6-phosphate, into the pentose phosphate pathway without necessarily altering the state of PFK. The gene discussed is SLC2A1; the disease is neoplasm.