Ijichi et al. [57] showed that several CXC chemokines secreted by the pancreatic ductal adenocarcinoma (PDAC) cells in K-ras+Tgfbr2KO mice induced connective tissue growth factor (Ctgf) expression in tumor-associated fibroblasts, which enhanced the growth of PDAC cell allografts but not the PDAC cells themselves; the tumor progression was attenuated by CXCR2 inhibition, which indicated that tumor-stromal interactions regulated tumor progression via a CXCR2-dependent chemokine and Ctgf axis. This evidence concerns the gene KRAS and neoplasm.