these neuroblasts into the marginal zone, it is theorized that VLDLR may encode a “stop signal.” This is supported by the fact that VLDLR is primarily expressed in the cortical plate adjacent to reelin-expressing cells, Cajal–Retzius cells, and in the intermediate zone. However, definitive evidence has not yet been found. In general, reelin binds VLDLR and undergoes endocytosis via clathrin-coated vesicles. Meanwhile, an intracellular protein, Dab1, has a PI/PTB domain that interacts with the NPxY sequence found in the cytoplasmic tail of VLDLR. As a result, Dab1 is tyrosine phosphorylated and reelin is degraded. Finally, phosphorylated Dab1 activates an intracellular signaling cascade that directs neuroblasts to their proper location through the alteration of the cytoskeleton. Many of the specifics of this pathway are still being investigated. It is not yet known if Dab1 is phosphorylated as a result of the endocytosis of reelin, or if there is another mechanism at play. In addition to the organization of the neocortex, VLDLR also plays a role in neuronal migration of the hippocampus and the Purkinje cells of the cerebellum. Yet, much information on this process is still unknown. Associated disorders Mutations within the VLDLR gene lead to a multitude of disorders of varying severities. These disorders are usually associated with cholesterol homeostasis or a disorganization of neuron ordering in the brain due to disruption of the reelin pathway. The most prominent of these diseases are type I lissencephaly, VLDR-associated cerebellar hypoplasia, and atherosclerosis. In contrast to causing diseases, VLDLR has also been identified as a possible remedy for some disorders. Implementation of VLDLR into the liver may cure familial hypercholesterolemia (FH) in patients who either have defective LDLR or have defective immune systems that attack this protein. Since VLDLR is non-immunogenic it does not initiate an immune response, thus it is able to function normally under defective immune systems. In addition, being that apoE, a major ligand of VLDLR, is a leading genetic risk factor for Alzheimer’s disease, VLDLR may play a role in modulating the risk of this disorder which is explained by the fact that a decrease in reelin signaling in the fascia dentata is supposed to initiate Alzheimer's disease. VLDLR has also been shown to reduce the chances of premature heart disease and stroke because VLDLR clears out lipoprotein A (Lp(a)), a major inherited risk factor for these diseases. Type 1 lissencephaly Type I lissencephaly, or agyria-pachygyria, is a