Huntington's disease is a hereditary neurodegenerative disease. The HTT gene mutation is based on increased CAG sequences, leading to an increased tendency to aggregate huntingtin protein (HTT) in brain neuron cells. The disease manifests itself in uncontrolled movements, problems in basic physical activities, and mental retardation. This paper presents an overview of Huntington's disease research. After the HTT gene was mapped on the fourth chromosome and successfully cloned, a whole series of research began on the mutation itself and its effect on the phenotype of the affected person at the molecular level. In the beginning, the treatment of this disease was limited to alleviating the symptoms, but various molecular treatment approaches were also tried, such as the targeted degradation of the mutated form of huntingtin or the silencing of its expression by the action of RNA or specific antibodies. Recently, efforts are being made to develop a gene therapy that could finally prevent the progression of this disease. Although therapies with DNA and RNA molecules and antibodies have shown some positive effects, the potentially best drug at this moment seems to be tominersen, an antisense specific oligonucleotide (ASO) that degrades mutated HTT, which is still in the phase II of clinical trial.