In a Huntington’s disease cell model, exposure to both physiological (1nM) and over-physiological (10 nM) Mn levels enhanced p-IGFR/IR-dependent AKT phosphorylation, and more than 70% of Mn-induced p-Akt signaling was dependent on p-IGFR rather than other upstream and downstream effectors [60]. This evidence concerns the gene AKT1 and juvenile Huntington disease.