For example, Duvick et al. [13] crossed f-ATXN1 mice to ACTA1-Cre, affecting muscle-restricted inactivation of mutant ATXN1 and preventing myopathy: offspring of f-ATXN1; ACTA1-Cre lacked muscle fiber atrophy and retained normal forelimb grip strength, whereas littermates with active mutant ATXN1 exhibited marked calf muscle wasting and weakness. Here, ACTA1 is linked to myopathy.