For example, the ability to pharmacologically activate NRF2 was shown to be suppressed in iPSC-derived NSCs from Huntington’s disease patients as compared to normal subject controls, although NRF2 induction did inhibit inflammatory cytokine production in primary mouse microglia and astrocytes from YAC128 HD mice, as well as monocytes from HD patients (Quinti et al., 2017). This evidence concerns the gene NFE2L2 and juvenile Huntington disease.