It is involved in development and progression of several cancers—it stimulates proliferation of CRC cells via the GHSR/Ras/PI3K/Akt/mTOR axis [98], GLUT-1-dependent proliferation of oral cancers [99], GHSR/NF-κB- and GHSR/PI3K/Akt-dependent migration and invasion of gastric [100] and pancreatic adenocarcinoma [101], and ERK2-dependent angiogenesis [102]. This evidence concerns the gene AKT1 and lip and oral cavity carcinoma.