In the article “Disease Progression in a Transgenic Model of Familial Amyotrophic Lateral Sclerosis Is Dependent on Both Neuronal and Non-Neuronal Zinc Binding Proteins,” by Krishna Puttaparthi, William L. Gitomer, Uma Krishnan, Marjatta Son, Bhagya Rajendran, and Jeffrey L. Elliott, which appeared on pages 8790–8796 of the October 15, 2002 issue, the preceding work of Nagano et al. [Nagano S, Satoh M, Sumi H, Fujimura H, Tohyama C, Yanagihara T, Sakoda S (2001) Reduction of metallothioneins promotes the disease expression of familial amyotrophic lateral sclerosis mice in a dose-dependent manner. Eur J Neurosci 13:1363–1370] was inadvertently overlooked. Puttaparthi et al. independently confirmed the protective effects of non-neuronal metallothionein-I and metallothionein-II in mutant Cu,Zn-superoxide dismutase (SOD1)-deficient mice, but have also extended analysis with regard to motor function, neuronal counts, and metallothionein-III-deficient mice.