The clinical spectrum of CNM is diverse among affected individuals, and ~60–80% of CNM can be explained by mutations in myotubularin 1 (MTM1),1 dynamin 2 (DNM2),2 bridging integrator 1 (BIN1),3 ryanodine receptor 1 (RyR1),4 voltage‐dependent L‐type calcium channel subunit alpha‐1S (CACNA1S)5 and striated muscle preferentially expressed protein kinase (SPEG).6 Here, DNM2 is linked to centronuclear myopathy.