Altogether, these findings support the interpretation that deregulation in the expression levels of HSPB8 might render motoneurons more vulnerable to proteotoxic insults, while its induction might protect against the toxicity exerted by aggregation-prone species, including DPRs, which accumulate with high frequency in ALS and FTD patients (Al-Sarraj et al. 2011). The gene discussed is HSPB8; the disease is amyotrophic lateral sclerosis.