Specifically, we found that MM cells co-cultured with 29b-DCs presented a reduction of the phosphorylation of ATM, ATR, of their downstream molecules CHK1 and CHK2 and of H2AX, the main double-strand break marker, in both protein and foci numbers (Figure 6B) as compared with MM cells co-cultured with NC-DCs. The gene discussed is ATR; the disease is Miyoshi myopathy.