Since NF‐κB activity can also contribute to developing chemotherapy resistance, inhibiting NF‐κB is a potential strategy for overcoming chemotherapy resistance in MM.[33] Prior research has demonstrated that NF‐κB directly activates POU2F2 transcription in other cancer cells, thus leading to POU2F2 overexpression.[34, 35] Its expression and binding activity to cis‐regulatory elements are associated with decreased patient survival.[36] Bortezomib mainly inhibits the activity of NF‐kB through the ubiquitin‐proteasome system (UPS), thus exerting an anti‐MM effect. The gene discussed is NFKB1; the disease is Miyoshi myopathy.