To investigate potential mechanisms underlying the effects of CSE and adipokines on NK cell function, we measured 1) levels of NK cell inhibitory (CD158a, CD158b and NKB1) cell surface receptors, 2) up-regulation of CD107a, CD107b and CD69 and 3) production of intracellular cytokines by NK cells in the presence or absence of CSE basally or after K562 tumour challenge. The gene discussed is KIR2DL1; the disease is neoplasm.