Moreover, given that AMPK is a crucial gerosuppressor (and tumor-suppressor) that impedes mTOR-driven geroconversion (and mTOR-driven malignant transformation) [1-17], small molecules capable of activating AMPK by altering the de novo synthesis of purine nucleotides such as AMP should be expected to not only inhibit the pro-aging activity of mTOR gerogenes but also prevent aging-related diseases, such as cancer. This evidence concerns the gene MTOR and neoplasm.