Alix and ESCRT proteins are required for membrane fission during viral budding and egress and during the abscission stage of cytokinesis. These common roles have suggested that Alix functions as an ESCRT protein, a conclusion challenged by the finding that unlike ESCRTs, which control the formation of multivesicular endosomes, Alix does not influence the degradation of the EGF receptor. We previously showed that Alix controls neuronal death by an unknown mechanism, but dependent on its interaction with ESCRT proteins. Since then, numerous reports have shown that ESCRTs participate in macroautophagy. Given the direct interaction between ESCRTs and Alix, together with the known contribution of autophagy to cell death, it was hypothesized that Alix controls autophagy and thereby cell death. Our recent published results show that this is not the case. ESCRT protein activity therefore needs Alix for viral budding and cytokinesis but not for autophagy. The function of ESCRT can thus be clearly be disconnected from that of Alix.