Interestingly, according to ChIP sequencing tracks in the University of California Santa Cruz (UCSC) genome browser (http://genome.ucsc.edu/cgi-bin/hgGateway) [35], the promoter region of GPR87 showed STAT3 binding elements, suggesting that tumor inflammatory microenvironment-mediated hyperactivation of JAK2/STAT3 signaling might contribute to GPR87 upregulation in pancreatic cancer. This evidence concerns the gene JAK2 and neoplasm.