A possible mechanism for the reactivation of the infection is that the anti-inflammatory cytokines interleukin 10 (IL-10) and transforming growth factor beta (TGF-β), produced by Hodgkin’s lymphoma cells, have inhibited the activity of phagocytic cells, thus allowing the proliferation of the N. nova [19]. This evidence concerns the gene TGFB1 and Hodgkins lymphoma.