Particularly, its post-trial analysis reported paradoxically enhanced survival benefit among pancreatic cancer patients with elevated level of the pro-inflammatory chemokine eotaxin (14.8 [10.1–20.5] months MOS in high eotaxin group versus 7.9 [5.9–11.3] months MOS in low eotaxin group; p = 0.0135) [94], which is known to elicit angiogenic responses in vivo [95] and a significant increase in endothelial NO production [96]. Here, CCL11 is linked to pancreatic neoplasm.