The mechanism proposed for this finding is based upon the fact that: 1) the MYC oncogene is an estrogen-dependent gene, transcriptionally regulated by ER in AI-resistant cells45; 2) upregulation of MYC was shown to be HER2-dependent (specifically via MAPK signaling and constitutive activation of ER); 3) MYC enhances glutamine uptake from the extracellular space in AI-resistant breast cancer cells through upregulation of the glutamine importer, solute carrier family SLC1A5; and 4) glutaminase, the enzyme responsible for converting glutamine into glutamate, is also regulated by MYC44. The gene discussed is ERBB2; the disease is breast cancer.