SUPT4H1 and Huntington disease: Our earlier findings that dissociation of the Pol II complex from DNA in template segments containing expanded TNRs is increased during Spt4 deficiency, and that interference with the function of Spt4 or SUPT4H decreases expression of genes containing expanded TNR regions in cultured cells—while not significantly affecting transcription of genes containing shorter TNRs or no TNRs at all [13]—have raised the prospect that targeting the function of SUPT4H may be a useful strategy for treatment of HD and possibly other TNR diseases.