The concordance between dietary fat, B(a)P dose, tumor load, invasive nature of adenomas, and the concentrations of the above-mentioned markers provide a compelling rationale that Western diet accelerates B(a)P-induced colon tumor formation and proliferation through enhanced insulin, leptin and other inflammatory molecules, which as a consequence may induce important signaling pathways such as PI3k/Akt and ERK1/2. The gene discussed is AKT1; the disease is colonic neoplasm.