By contrast, mice in which the Flnc exons encoding Ig-like domains 21–24 were deleted (Flnctm1Lmk, http://www.informatics.jax.org/allele/key/35197) display neonatal lethality caused by defects in primary myogenesis [14], while inducible cardiac-specific ablation of Flnc expression resulted in embryonic death, or death associated with dilated cardiomyopathy in adult mice, respectively [92]. The gene discussed is FLNC; the disease is dilated cardiomyopathy.