SUPT5H and Huntington disease: Mutant alleles in most HD patients do not contain repeats of the length necessary to yield HD-related phenotypes in transgenic mice [48,49]; and additionally, the consequences of Supt4h knockdown potentially may be affected by genetic variation in the native cellular abundance of SUPT4H (and perhaps of SUPT5H its transcription elongation complex partner) in brain tissues of different individuals.