Mutations in the TTN gene coding for titin, a giant protein that works as a nano-spring, account for most known genetic forms of DCM (19–25% of familial forms and 11–18% of sporadic forms), with incomplete penetrance and variable expression, frequently (but not always) presenting with relatively mild phenotypes and slow progression (Bondue et al., 2018). The gene discussed is TTN; the disease is familial dilated cardiomyopathy.