The absence of a clear role for the Fas apoptosis pathway in T. brucei induced transitional B-cell death is particularly surprising, taken that (i) Fas upregulation on these cells is reported here to be a clear hallmark of progressing infection, and (ii) that Fas-FasL B cell killing in the context of an infectious disease has previously been described in the case of Trypansosoma cruzi infections, which induce Fas-mediated fratricide of IgG+ B lymphocytes specific for parasite antigens but not self antigens [27]. The gene discussed is FASLG; the disease is infectious disease.