It is regarded as a bidirectional spring that provides mechanical support to the sarcomere but also receives incoming signals.1 With the advent of next-generation sequencing, it became clear that truncating variants in TTN are found in 20% to 30% of patients with a dilated cardiomyopathy (DCM).2 While the role of TTN in cardiomyocyte function and structure is well established, far less is known about the possible regulatory roles of the RNA transcript (>100 kb) that TTN produces. The gene discussed is TTN; the disease is familial dilated cardiomyopathy.