Based on these observations, the authors develop an interesting hypothesis that could explain the unique lymphoma nature of cancers that developed in a deficient FasL/Fas context: since B lymphoma cells could behave as APC, T cells bearing a low affinity TCR for self-ags eliminate through a FasL/Fas system the developing B lymphoma cells, an elimination that cannot be taken over in lpr and gld mice or in ALPS patients. Here, FASLG is linked to autoimmune lymphoproliferative syndrome.