In addition, the discrepancies in the association of leptin genetics, obesity, and CRC may be explained by the insufficient sample size, statistics, genotyped markers, allele frequencies in various populations, linkage disequilibrium, or diet and lifestyle factors [99], emphasizing the need to assess LEP and LEPR gene variants in larger studies, including both obese and lean subjects, with epidemiologic data on dietary habits in different ethnicities. This evidence concerns the gene LEPR and colorectal carcinoma.