Huntington’s disease is a neurological disorder caused by an expansion of CAG repeats in the Huntingtin gene. The number of CAG repeats dictates the rate of progression of pathogenic events leading to onset of the disease. In this study, we investigate the transcriptional landscape of the disorder, using RNA-seq, in four human pluripotent stem cell (hPSC) lines differentiated to four cell types (neural progenitor cells (NPCs), mature neurons, hepatocytes and myotubes) with CAG repeats ranging from normal to juvenile onset (30-80 CAG repeat range). Despite being a predominantly neurological disorder, we see systemic effects, with ~20% and ~40% of expressed genes in myotubes and hepatocytes showing significant differential expression across the CAG repeats, and there is a higher proportion of genes which are significantly differentially expressed within a single cell type as opposed to multiple types. We also find clusters of differentially expressed genes in individual cell types that are enriched for functional categories but do not show a dose-dependent relationship with the CAG length and severity/age of onset. Several of these genes that do not show this correlation between gene expression and CAG length also exhibit the same relationship at the protein level. Finally, the transcriptional data along with the cell lines will be made available as a public resource.