The first is that the binding of the terminal phospholipids alters the conformation of the active sites, implying that the tunnel acts as an effector, only allowing the enzyme to be active in certain areas of the cell. The second hypothesis postulates that the tunnel regulates lipid membrane rigidity through its degradation of phenolic hydrocarbons and ability to bind to other lipids. Studies have shown that phenolic hydrocarbons affect the functional and structural properties of cell membranes.
One theory posits that the attachment of phospholipid molecules to the enzyme changes its shape, suggesting that the tunnel functions as a regulator, only permitting the enzyme to be active in specific regions of the cell. The second hypothesis proposes that the tunnel regulates membrane stiffness through its degradation of phenolic compounds and binding to other lipids.