LEP and neoplasm: With the overproduction of leptin and a functional increase in estrogen derived from adipose tissue, there is an increase in signals to the nucleus with the activation of oncogenic pathways such as NF-κB, AP-1, PI3K, STAT3, AKT, and JAK-1, thus leading to the release of proinflammatory proteins such as TNFα, IL-1, and IL-6, these changes are recognized as processes of low-grade local inflammation until they progress to systemic inflammation with the generation of reactive oxygen species and the promotion of tumor cell growth [9].