In this light, it has been shown that more than 1000 transcripts express aberrant isoforms in ischaemic and dilated cardiomyopathies, indicating that alternative splicing is a highly regulated process and an important layer of gene regulation during pathological remodelling of the heart.50,51 It will be very interesting to see whether therapeutic up-regulation of QKI using gene therapy in acquired heart disease will be able to shift splicing towards more cardioprotective isoforms and improve cardiac remodelling and function. This evidence concerns the gene QKI and dilated cardiomyopathy.