Supporting the idea that interrupting the Torsin/cofactor interaction is detrimental are reports of patients with mutations in the LAP1 gene, TOR1AIP1, who display dystonic-like symptoms [15,68], cardiomyopathy [14,15,68,69], deafness [14,68], and muscular dystrophy [16,69] (Figure 2A). Here, TOR1AIP1 is linked to cardiomyopathy.