In turn, Futenma et al. examined SOD-1 isomers and showed that despite a decrease in Cu/Zn-SOD tetramers or octamers, a significant increase in SOD-1 levels was observed in patients treated with HD due to an increase in SOD-1 monomers (which are immunologically active but enzymatically inactive) [42]. The gene discussed is SOD1; the disease is Huntington disease.