Whereas KMS11 (Fig. 2A), MM1R, H929, and RPMI-8226 (Supplementary Fig. 2A) maintained high levels of DNA damage activation and had significantly increased rates of apoptosis after 3 weeks of ILF2 ASO, JJN3 cells overcame ILF2 ASO−induced DNA damage activation and became resistant to ILF2 ASO treatment (Fig. 2B), which suggests that MM cells can eventually activate compensatory mechanisms to overcome the deleterious effects of DNA damage and maintain their survival. The gene discussed is ILF2; the disease is Miyoshi myopathy.