Although our study did not definitively identify a common or first event of genetic and/or epigenetic alteration establishing NE clonality, from a mechanistic point of view, KRAS or PIK3CA mutation would be considered likely to provide NE cell clones with the ability to proliferate and invade neighboring NM and/or other organs, driving the development of adenomyosis. The gene discussed is KRAS; the disease is nemaline myopathy.