Examples include ARID1A (AT-rich interaction domain 1A) that was detected in a pedigree analysis implicating DNA repair and chromatin remodeling in MM risk (Waller et al., 2018) and EP300 (E1A binding protein p300) (Bolli et al., 2017), which encodes a histone acetyltransferase (HAT) that regulates transcription via chromatin remodeling. This evidence concerns the gene ARID1A and Miyoshi myopathy.