The loss of expression of differentiation markers in CAAs such as adiponectin or leptin and the increased secretion of proinflammatory cytokines as Interleukin 6 (IL-6) and tumor necrosis factor (TNF) generate a permissive niche for tumor growth and dissemination by stimulating adhesion, migration, and invasion proprieties of malignant cells (Figure 1). The gene discussed is LEP; the disease is neoplasm.