Eight proteins involved in leukocyte transendothelial migration were increased in abundance in EMM (PECAM1, ITGB1, ACTB, ACTN1, VASP, VCL, RAP1B, RAC1, ROCK2) and may indicate a potential mechanism by which specific MM clones exit the bone marrow niche during extramedullary transition. This evidence concerns the gene ACTN1 and Miyoshi myopathy.