MYL1 and cardiomyopathy: The RMS patients in this dataset are likely to be congenital (due to up-regulation of mutated TNNT1 stimulated by FGFR4 and suppression of anti-proliferative effects of RA in FHL3, RXRG, MYL1 and RND3) and these patients have a lower risk of developing cardiomyopathy (due to over-expression in TNNT2, BIN1, SEPT4 and HSPB2 potentially suppress the expression level of FNDC5).