CCL2 and pancreatic ductal adenocarcinoma: Another study using the KRAS/p53 mutant pancreatic ductal adenocarcinoma model found that active YAP contributes to the differentiation and accumulation of MDSC in tumor microenvironments by promoting the expression and secretion of multiple cytokines and chemokines, including CXCL1/2 and C-C motif chemokine 2 (CCL2) [84].