Another peculiarity of MLP is that it can shuttle from the cytosol to the nucleus where it serves as a scaffold protein to adapt transcription factors to their DNA-binding sequences.2, 3 In fact, MLP is involved myocyte differentiation by activating transcription factors such as MyoD, myogenin, etc.4 To this effect, mutations in the N-terminal region of MLP have been linked to the development of dilated cardiomyopathy (DCM) or hypertrophic cardiomyopathy (HCM). The gene discussed is CSRP3; the disease is familial dilated cardiomyopathy.