Additionally, given glucose's efficacy in stimulating expression of the insulin receptor (IR) as well as modulating its affinity for insulin, hyperglycemia, and hyperinsulinemia are speculated to promote cancer development and proliferation via activation of IR and downstream provocation of the PI3K-Akt-mTORC1 and MAPK pathways (5, 6) Furthermore, proliferation of lung cancer cells correlates with uptake of the glucose-based tracer [F-18] fluorodeoxyglucose during positron emission tomography (PET) scans (7). This evidence concerns the gene INSR and Hyperinsulinemia.