The first exon of the HTT (Huntingtin) gene has an aberrant increase of CAG repeats, which causes Huntingtin's disease, a neurological illness disease called Huntingtin. This genetic anomaly leads to creation of an aberrant protein of Huntingtin protein called as (Htt) which has extended poly-glutamine sequences of varying lengths, which aggregate and become toxic to the brain, causing significant damage. Although the exact role of the HTT gene is unknown, it is known to be essential for the prenatal development of neurons in the brain. While thorough reversal for the damage of brain is currently beyond our capabilities, there is promising research engrossed treatments based on peptide for Huntingtin, including both polyglutamine and non-polyQ peptides such as QBP1, P42, ED11, and BIP.By focusing on different areas of the Htt protein, these peptides—QBP1 and P42 in particular—avoid aggregation. P42 ties to residues between 480 and 502, while QBP1 interacts with several locations within the Htt protein's N-terminal section.