Mature lymphocytes and peripheral lymphoid organs show a characteristic pattern of ERM protein expression, with moesin expressed at three fold higher levels than ezrin, and little to no radixin expressed. In contrast, we find that ezrin expression is higher in the thymus, where it is roughly equimolar with moesin. Real-time PCR analysis showed that ezrin and moesin are differentially regulated during development, with ezrin expression highest in early thymocytes, and moesin highest in mature thymocytes and peripheral T cells. Assuming that expression of these proteins is controlled at the mRNA level, then ezrin is expressed at levels equal to or higher than moesin in early thymocytes, and the 3:1 moesin:ezrin pattern characteristic of mature T cells emerges late in development. In keeping with this, our histological analysis shows strong ezrin expression in the thymic cortex, where early T cell development takes place, and strong moesin expression in the medulla, which is enriched in more mature T cells. Interestingly, ezrin mRNA levels diminish sharply between the DN3 stage and the ISP stage of development, at the time when the pre-TCR is expressed and positive and negative selection occurs. It is also at this stage of development that moesin levels begin to rise. This raises the possibility that the switch in ERM protein expression is triggered by pre-TCR signaling and thymic selection. In addition, the absence of co-localization suggests that Spod-11tox is not involved in non-self-recognition. We considered the possibility that whether or not the enhanced physical activity and associated energy expenditure accounted for every extra calorie expended in the lean rats may not be the crucial question. It is possible that high physical activity and high aerobic capacity are key, interrelated features of the lean phenotype. This may allow us to more effectively target the fundamental physiological traits and genetic differences underlying leanness. First, however, it was necessary to establish that this effect generalized to human physiology and behavior and was relevant to human health. If endurance capacity, not body size, is a major factor determining daily activity levels, then the effect we identified in rats should generalize: people with high intrinsic running endurance should also have high daily activity levels. Moreover, if endurance and the Ponatinib Src-bcr-Abl inhibitor tendency to be active are linked at the mechanistic level, then we would expect this association to overshadow the association between daily activity and body weight, as it did in rats. Like spontaneous activity, inborn exercise capacity varies considerably among people, but why some people have higher inborn endurance than others is complex. This is supported by immunolabelling experiments showing that, in vitro, rSpod-11-tox does not directly interact with E. coli or P. pastoris.