AKT1 and neoplasm: Tumor cells resist anoikis through multiple mechanisms (Fig. 5): extracellular factors such as degradation and remodeling of ECM, significant expression of ECM, and transforming growth factor β; cytosolic factors including continuous alteration of integrins, calmodulin, and altered expression profiles of EGFR and ERBB2; intracellular factors involving the alteration of intracytoplasmic components (e.g., FAK, Src, connexins), abnormal activation of pathways (e.g., PI3K-Akt, Mek/Erk, NF-κB), and expression profiles of anoikis-related proteins (BCL2 family, P53, zinc catalase, ferritin).