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Some genetic abnormalities of multiple myeloma (MM) detected more than two decades ago remain major prognostic factors. In recent years, the introduction of cutting-edge genomic methodologies has enabled the extensive deciphering of genomic events in MM. While the precise mechanisms driving MM pathogenesis remain under investigation, substantial evidence suggests that genetic and epigenetic alterations play a crucial role in disease initiation and evolution. Multiple myeloma occurs due to acquisition of molecular and genetic aberrations, leading to the initial asymptomatic premalignant proliferation of plasma cells, referred to as monoclonal gammopathy of unknown significance (MGUS). Multiple myeloma arises from acquired genetic changes, known as somatic mutations, within the plasma cells themselves. These changes occur during a person’s lifetime and are not passed down through generations. Primary genetic events divide multiple myeloma into 5 subgroups based on the presence of 1 of 3 types of recurrent immunoglobulin heavy chain gene translocations, hyperdiploidy, or of neither of these.