Cadmium, an environmental pollutant, is bad news for the testis. One of its effects is to disrupt the tight junctions formed by the Sertoli cells in the seminiferous tubules. These tight junctions form the blood-testis barrier (BTB) and, when this barrier is disrupted, germ cell numbers are reduced and infertility results. Now Yan Cheng and colleagues have harnessed the deleterious effect of cadmium to find out how the extensive restructuring of the BTB necessary for normal spermatogenesis is controlled (see p. 783). They show that in rats the cadmium-induced disruption of the BTB (as measured by the loss of the occludin and zonula occludens 1 proteins from tight junctions) is mediated by the TGFβ3/p38 MAP kinase signalling pathway. The primary loss of BTB function leads to a secondary disruption of adherens junctions in the testis - adherens junction dynamics are also regulated by TGFβ3/p38 MAP kinase signalling. Finally, the researchers propose that the protease inhibitor α2-macroglobulin plays a crucial role in tight junction and adherens junction dynamics in the testis by interacting with TGFβ3.