DNM1L and systemic lupus erythematosus: This has been attributed to an imbalance of mitochondrial biogenesis36 and turnover by mitophagy.37 Specifically, our previous studies of SLE T cells have demonstrated human retrovirus endogenous sequence (HRES)-1/ras-related protein 4 (RAB4)-mediated depletion of dynamin related protein 1 (Drp1), a mediator of mitochondrial fission.36 The accumulation of mitochondria in lupus T cells is sensitive to mTOR blockade, with clinical benefit in patients38 and mice39 with SLE.