HSPB8 and amyotrophic lateral sclerosis: HSPB8 overexpression rescues from protein accumulation and aggregation of mutant SOD1 and TDP-43 in cell models of ALS (Crippa et al., 2010a,b), while its silencing has opposite effects favoring misfolded proteins accumulation in motor neurons (Crippa et al., 2010a,b).