The genetic background of Huntington's disease (HD) is primarily characterized by a mutation in the HTT gene, which is located on the short arm of chromosome 4 (4p16.3). The genetic mutation responsible for HD involves an abnormal expansion of a trinucleotide repeat sequence, known as CAG, within the HTT gene. The CAG repeat encodes a polyglutamine tract in the huntingtin protein. In individuals with HD, the CAG repeat is expanded beyond a certain threshold, resulting in an increased number of glutamine residues in the huntingtin protein. HD follows an autosomal dominant pattern of inheritance, meaning that a person who inherits a single copy of the mutant HTT gene from one parent will develop the disease, regardless of whether the other parent carries the mutation. Each child of an affected individual has a 50% chance of inheriting the mutated gene. A notable feature of HD inheritance is anticipation, where the age of onset of symptoms tends to decrease and the severity of symptoms tends to increase in successive generations. This phenomenon is thought to be due to further expansion of the CAG repeat during transmission from one generation to the next. While the presence of an expanded CAG repeat in the HTT gene is necessary for the development of HD, the age of onset and severity of symptoms can vary widely among individuals with the mutation. Some individuals may carry the mutation but never develop symptoms (referred to as incomplete penetrance), while others may have an earlier onset and more severe disease. In addition to the CAG repeat expansion in the HTT gene, other genetic factors may influence the age of onset and progression of HD. Genetic modifiers, such as variations in other genes or non-genetic factors, may interact with the mutant HTT gene to modify disease onset, severity, and progression. Research into genetic modifiers may provide insights into the variability of HD phenotypes and identify potential targets for therapeutic intervention. While the role of HTT in HD is well-established , we wished to collate a comprehensive list of other genes that might play a role in the development of HD. Results from our anlysis are visualized in Figure . Besides HTT, other genes that might play a crucial role in the eitology of HD include BDNF, NPY, SIRT1, HAP1, PPARGC1A, JPH3, GRIN2B, CNTF, and IGF1. A comprehensive table, including extensive details regarding genes, related proteins, expression profiles, function, and other diseases, as well as multiple examples, is included in the Supporting Information, Table ) Genetic testing for the CAG repeat expansion in the HTT gene can confirm the diagnosis of HD in individuals with symptoms or a family history of the disease. Predictive genetic testing can also be offered to individuals who are at risk of inheriting the mutation but do not yet have symptoms. Genetic counseling is recommended for individuals considering testing to discuss the implications of the test results and the potential impact on themselves and their families. Understanding the genetic basis of HD is essential for accurate diagnosis, genetic counseling, and the development of targeted treatments for this devastating neurodegenerative disorder.