Multiple myeloma (MM) is the second most common hematologic malignancy and is characterized by the expansion of clonally plasma cells and related organ or tissue damage.1 The clinical behavior, response, and survival of MM are heterogeneous, and much of this variability may be driven by acquired genetic factors, including primary immunoglobulin translocations, hyperdiploid, and additional copy number gains and losses.2 The abnormalities of chromosome 1q (+1q) were found in about 30%–40% of patients with newly diagnosed MM and at a higher proportion at the refractory/relapse stage.3 The gain/amplification of 1q (1q gain/amp) has been reported to relate to poor outcomes due to the dysregulation of lots of genes located in 1q including CKS1B, ANP32E, and ADAR1.3 However, the other prognostic genes on 1q and the underlying mechanisms remain elusive.