The work suggests that the substantial lactate generated by glycolysis in blood-dwelling schistosomes can be excreted across the parasite tegument via the tegumental membrane protein SmAQP. These data provide a molecular understanding of how schistosomes cope with the large quantities of lactate generated from the largely anaerobic carbohydrate metabolism that is a hallmark of their intravascular lives. Caspase-8 is an initiator protease recruited to the death inducing signaling complex during apoptosis initiated by death receptors. Homotypic interactions, mediated by the aminoterminal death effector domains of caspase-8, are required for recruitment and subsequent maturation and dimerization of caspase-8 initiating the extrinsic apoptosis cascade. In addition to this role in death receptor-mediated apoptosis, cumulative evidence suggests that caspase-8 performs other non-apoptotic functions in development, including proliferation, cell migration and differentiation. We and others previously reported that caspase-8 has the capacity to localize to a number of different cellular locations, including the cytosolic compartment, actin-rich Fangchinoline ruffles, endosomes, including those at the front of migrating cells, focal adhesions and stable microtubule structures, such as centrosomes. Interestingly, the different domains of caspase-8 appear to favor localization to different cellular compartments. It is possible that these different preferred locations may ultimately influence caspase-8 function. Differentiation, senescence, and apoptosis are critical programs for the development and maintenance of cellular homeostasis. Disruption of any of these Araloside-V essential processes is an important component in the pathogenesis of many diseases, including cancer. A common characteristic of human cancer is disrupted cellular differentiation. In some cancer cells, the induction of differentiation with therapeutic agents terminates uncontrolled proliferation. Even among therapies which do not aim to specifically induce cell differentiation or senescence, it nonetheless appears to be a common mechanism limiting tumor growth.