Also, in Huntington’s disease, REST is believed to be sequestered to the cytoplasm due to the complex formation between cytoplasm residing huntingtin and huntingtin-associated protein 1 (HAP1) further interacting with REST-interacting LIM domain protein (RILP), while this is reversed in mutant huntingtin mouse models leading to RLIP mediated enhanced translocation of REST to nucleus and repressive action [75,76,77]. This evidence concerns the gene HTT and Huntington disease.