Thisdisease is characterized by high genome instability; hence, SIRT6overexpression may be a compensatory response to facilitate DNA repair.While this mechanism may be favorable for cancer cell survival, Ceaand colleagues demonstrated that in MM cells, SIRT6 interacts withELK1 and deacetylates H3K9 at the promoters of MAPK signaling genes,thus stopping cell proliferation. This evidence concerns the gene SIRT6 and Miyoshi myopathy.