To investigate general mechanisms in proteostasis across different cardiomyopathy models, we examined two established models of desmin-related cardiomyopathy (DesD7-TG and CryABR120G-TG [12,13]) together with Myozap-TG mice, which we have previously shown to develop a phenotype characterised by protein aggregation and cardiomyopathy, independent of desmin-related pathology [14,15]. This evidence concerns the gene MYZAP and cardiomyopathy.