Mechanistically, CD44 promotes tumor growth via the activation of mitogen-activated protein kinases (MAPK) and phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signalling pathways and accelerates epithelial-to-mesenchymal transition (EMT) by activating AKT signalling, which results in the formation of EMT-associated recurrent tumours and apoptosis resistance [45]. The gene discussed is AKT1; the disease is neoplasm.