CPZ-induced oxidative stress in the brain exhibits a relatively selective detrimental effect on oligodendrocytes (Ludwin et al. 1978), and initiates a cascade of pathogenic events including oligodendrocyte apoptosis, microglial and astroglial activation, and demyelination; resulting ultimately in MS-resembling pathology in animals (Acs and Kalman 2012; Praet et al. 2014; Omotoso et al. 2018). This evidence concerns the gene CPZ and myeloid sarcoma.