In this study, we used a collection of human isogenic cell lines that vary in their HTT genetic makeup (WT 20CAG/20CAG, heterozygous 20CAG/-, HTT-KO −/−, and HD 72CAG/20CAG) to systematically investigate the genetic mechanism behind HD phenotypes in previously described in vitro micropattern-based assays of activin signaling transduction and self-organized neuronal organoids (Haremaki et al., 2015; Galgoczi et al., 2021). The gene discussed is INHBE; the disease is Huntington disease.