FHL1 and amyloidosis: Aggresomes, constantly evolving structures capable of recruiting ubiquitination enzymes, chaperones and proteasome components [38] have been found in other pathological conditions characterized by the formation of protein aggregates, namely in Alzheimer’s, Parkinson’s and Huntington’s diseases; amyloid and prion disease [38,39]; in hereditary reducing-body myopathy [40] and in a sarcopenic patients with rigid spine syndrome and a mutation in the FHL1 gene [41].