SOD1 and amyotrophic lateral sclerosis: Administration of the BH4 domain of BCL-X(L) fused to the protein transduction domain of the HIV-1 TAT protein was sufficient to restore Ca2+ homeostasis in astrocytes overexpressing the ALS-associated SOD1 (G93A) mutation, and chronic treatment of SOD1(G93A) transgenic mice with the TAT-BH4 peptide delayed the onset of the disease and improved motor function and lifespan (Martorana et al., 2012).