rare developmental disorder characterized by the absence of gyri and sulci in the brain. These severe malformations are a result of aberrant neuronal migration. In classical type I lissencephaly, neuronal migration begins but is unable to continue to completion. This process is likely disrupted by alterations to several genes, including the VLDLR, DCX, ARX, TUBA1A, RELN and LIS1. The severity of type I lissencephaly therefore varies with the mutation type. A homozygous deletion affecting the VLDLR gene results in a low degree of cortical thickening and absence of a cell-sparse zone. The cell-sparse zone describes the region between the outer and inner cortical layers of arrested neurons. In addition, type 1 lissencephaly is closely associated with cerebellar hypoplasia. VLDLR-associated cerebellar hypoplasia Disequilibrium syndrome (DES) was first described in the 1970s as a non-progressive, neurological disorder. In a 2005 study, DES was renamed as VLDLR-associated cerebellar hypoplasia (VLDLRCH) after its cause was linked to a disruption in the VLDLR gene. At least six mutations affecting the homozygous recessive allele of the VLDLR gene have been identified and found to cause VLDLRCH. Several of these mutations have been localized to specific exons encoding the gene. One such mutation is a cytosine to thymine transition at base pair 1342 in exon 10 that causes a substitution at Arg448 for a termination signal. Likewise, there is evidence of a cytosine to thymine transition at base pair number 769 in exon 5 that causes a substitution at Arg257 for a termination signal. A third known mutation is caused by a homozygous 1-base pair deletion in exon 17 that causes a frameshift and premature termination in the O-linked sugar domain. All such alterations to the VLDLR gene prevent the production of VLDLR and are therefore termed loss-of-function mutations. The recognized symptoms of VLDLRCH are moderate-to-severe intellectual disability, seizures, dysarthria, strabismus and delayed locomotion. In some cases, children with VLDLRCH learn to walk very late in development after the age of six years, or never learn to walk independently. The frequency of this disorder is unknown because early diagnosis of VLDLRCH is difficult using imaging techniques. It is associated with parental consanguinity and found in secluded communities such as the Hutterites and inbred families from Iran and Turkey. Atherosclerosis Atherosclerosis is marked by an excessive accumulation of cholesterol by macrophages, leading to their transformation into foam cells. This accumulation of cholesterol is caused by dysregulation of cholesterol