Here, haploinsufficiency (20CAG/-) did not fully recapitulate the HD-signature phenotypes previously described for HD (72CAG/20CAG) and HTT-KO hECSs in these assays (Figure 1), indicating that the molecular insult due to the presence of mutant HTT in our model cannot be explained by a simple loss-of-function mechanism. Here, HTT is linked to Huntington disease.