The activation of AhR by either an exogenous (TCDD) or endogenous ligand (FICZ) increased the level of TDP-43 protein in human neuronal cell lines (BE-M17) and motor neurons differentiated from iPSCs; however, the observed effects were reversed by AhR antagonists, suggesting that exposure to environmental toxins that activate AhR can be a risk factor for ALS development/progression [145]. Here, AHR is linked to amyotrophic lateral sclerosis.