To date, the precise mechanism by which these treatments may have facilitated the pathogenesis of PML is a matter of debate, but likely it is based on leukocytes inability to traffic to the sites of JCPyV reactivation and infection, and on trafficking of JCPyV latently infected B cells and/or haematopoietic precursors CD34+ between the BM and the brain. This evidence concerns the gene CD34 and progressive multifocal leukoencephalopathy.