The latter results are consistent with our recent findings [55], whereby enolase I expression is inversely linked to P-gp expression, and drug resistant P-gp-expressing tumor cells escape tamoxifen sensitivity by down-regulating P-gp expression to decrease their ATP requirement to fuel P-gp function (e.g., ATP production through oxidative phosphorylation) with a consequent rise in enolase I function (ATP production through glycolysis). The gene discussed is PGP; the disease is neoplasm.