Nonetheless, some focused m6A activity appears indispensable for postnatal cardiac development as heart-specific conditional knockout YTHDC1 m6A reader protein has been described to result in premature death of mice at 2–3 months of age due to disrupted m6A-dependent splicing of Titin pre-mRNA, accompanied by destructed sarcomere organization, DCM, and ultimately HF.150. This evidence concerns the gene TTN and familial dilated cardiomyopathy.