Tigecycline has been demonstrated to induce autophagy in gastric cancer cells.7 To explore whether autophagy is also functionally involved in tigecycline‐induced cytotoxicity, we analysed the expression levels of LC3 and SQSTM1/p62 and found that tigecycline dose‐dependently promoted the accumulation of LC3 II and subsequently degraded the autophagy substrate SQSTM1/p62 in MM cell lines RPMI‐8226, NCI‐H929 and U266 (Figure 3A), indicating that autophagy does occur in tigecycline‐treated MM cells. The gene discussed is MAP1LC3A; the disease is Miyoshi myopathy.