This is supported by studies indicating that these tumours are associated with molecular alterations of key developmental signalling pathways, including the enhanced activation of the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) and the phosphoinositide 3-kinase/Protein Kinase B/mechanistic target of rapamycin (PI3K/AKT/mTOR) pathway [1, 8–11]. This evidence concerns the gene AKT1 and neoplasm.