A large panel of adipokines, including leptin, adipokine, chemerin, apelin, omentin-1, vistatin, nesfatin-1, and other pro-inflammatory cytokines (IL-6 and TNF-β) produced by excessive PRAT may contribute to tumor progression by inducing a pro-inflammatory, dysmetabolic, and pro-angiogenic tumor microenvironment [3,16,17,40,41]. The gene discussed is NUCB2; the disease is neoplasm.