In this study, we found that LMNA bound to total and phosphorylated (S62, T58) forms of c‐Myc at nuclear periphery or intranuclear foci, and repressed the roles of c‐Myc in increasing expression of EPRS and LARS, providing a therapeutic approach targeting c‐Myc within tumours. The gene discussed is MYC; the disease is neoplasm.