While in the majority of MM cases overexpression of CCND1 can be explained by somatic structural variants i.e., juxtaposition to IGH enhancer or chr11q25 gain31, such aberrancies do not account for overexpression of CCND2. Our identification and functional validation by complementary approaches of the distal cis and trans regulators of CCND2 expression addresses this gap in the biology of MM and allowed further insights into how the activity of this enhancer is regulated in different myeloma genetic subgroups. The gene discussed is CCND1; the disease is Miyoshi myopathy.