This is consistent with the clinical observation that in MGUS patients higher levels of M protein are associated with increased risk of transformation to MM.34 Additionally, reduced level of oxidative phosphorylation and decreased oxidative stress have been shown to suppress mitophagy and decrease susceptibility to apoptosis.35 Recently, Jin et al. found that the AAA+‐ATPase Atad3a suppresses Pink1‐dependent mitophagy and maintains hematopoietic homeostasis.36 The gene discussed is PINK1; the disease is Miyoshi myopathy.