These clinical observations prompted further mechanistic studies demonstrating that chemerin promotes epithelial–mesenchymal transition (EMT), migration, and invasion of gastric adenocarcinoma (AGS) cell lines via both GPR1 and CMKLR1, through activation of the mitogen-activated protein kinase (MAPK), Ras homolog family member A/Rho-associated protein kinase (RhoA/ROCK), and protein kinase C (PKC) signaling pathways. Here, RHOA is linked to gastric adenocarcinoma.