As examples, eight patients with core myopathy had pathogenic variants in RYR1, eight NM cases harbored the typical compound heterozygous combination of a nonsense or a frameshift variant with a splice site variant affecting an in-frame exon of NEB. We also detected heterozygous missense variants in the highly conserved ACTA1 gene in five patients with classical NM and nemaline rods on muscle sections. This evidence concerns the gene ACTA1 and nemaline myopathy.