In the present study co-over-expression of UNC-45 with disease-causing PolyQ-72 dramatically reduced amyloid aggregate density (Figure 7L and 7M) and ameliorated cardiac dysfunction by decreasing the incidence of cardiac arrhythmia, suppressing the mutant-Htt-induced cardiac dilation (Figure 7A, 7B) and improving cardiac contractility to a dramatic extent (Figure 7C). The gene discussed is HTT; the disease is cardiac rhythm disease.