The first 2 cases of paradoxical disease activation in patients with MS treated with alemtuzumab were reported in 2017.1 The authors proposed that a secondary B cell–driven autoimmune disease targeting the CNS and appearing similar to MS could occur after alemtuzumab therapy due to the observation that B-cell numbers recover far more quickly after alemtuzumab than CD4+ and CD8+ T cells, sometimes overshooting pretreatment levels.1 However, the relative kinetics of B- and T-cell recovery have no effect on the risk of non–CNS-directed autoimmunity. Here, CD8A is linked to myeloid sarcoma.