To test the relative contributions of these genes to MM formation, one study used mice with heterozygous deletions of Cdkn2a exon 1α (resulting in loss of p16Ink4a) or exon 1β (p19Arf), or with a deletion of exon 2 (deleting both p16Ink4a and p19Arf) (51). The gene discussed is CDKN2A; the disease is Miyoshi myopathy.