Our identification of TGFβ signalling as a significantly altered pathway in a cell model of HD is consistent with a recent RNA-seq analysis of HD patient iPSC-derived NPCs, where TGFβ signalling was one of the most significantly dysregulated pathways [11], and targets of SMAD3 were over-represented within genes differentially expressed between HD-NPCs and their isogenic controls [11]. This evidence concerns the gene TGFB1 and Huntington disease.