Contrarily, in cells isolated from the primary tumor and lung metastasis tumor, H19 regulates GIT2 via sponging miR-200b/c and promotes G protein-coupled receptor kinase interacting protein 2 (GTI2; one of ArfGAPs) expression through inactivating ARF [63]; thus, MET took place in order to accelerate successful metastatic colonization of a secondary organ [64,65]. The gene discussed is MET; the disease is neoplasm.