People with high body mass index (BMI) are at a greater risk for developing cancer as indicated by the aggregate of epidemiological studies. As the BMI elevates from normal to overweight to obese categories, there is a “dose-response” effect with the growing risk. The future risk is reduced through fruitful continual weight loss. Numerous large cohort studies and two meta-analyses of cohort and case-control studies have reinforced the correlation between overweight and the risk of leukemia in the aggregate. One of the two meta-analyses found an increased risk for all four major subtypes of leukemia. A meta-analysis of 13 cohorts and nine case-control studies supported the strong relationship between higher BMI and the risk for non-Hodgkin’s lymphoma, especially the risk for diffuse large B-cell lymphoma. A meta-analysis of eleven cohorts and four case-control studies concluded that the risk of myeloma rises as BMI increases. It remains uncertain whether there is any biological relationship between obesity and the risk for cancer. The two significant causal pathways could be either “inductive” or “selective.” The induction of neoplastic transformation may be favored because of a rise in cell mutation rate, dysregulation in gene function, disturbance in DNA repair, or because epigenetic changes were induced (inductive). These can occur because of the metabolic, endocrinologic, immunologic, and inflammatory-like changes resulting from obesity. Or, an environment might have been formed by obesity that lets dormant pre-existing clones materialize (selective).