Renal fibrosis is characterised by tubular atrophy and apoptosis of tubular epithelial cells, but the underlying mechanisms are unclear. microRNAs (miRs) have been shown to be involved in apoptosis in cancer cells, in particular those of the miR-34 family. On page 4494, Chunsun Dai, Junwei Yang and colleagues thus asked whether miR-34a, which is widely expressed in mammalian cells, might also have a role in fibrosis progression. Using fibrotic kidney induced by unilateral ureteral obstruction as their experimental system, they observe that miR-34a is upregulated in the tubulointerstitial space and in microvesicles that they isolate from the kidney tissue. Interestingly, miR-34a is, however, not synthesised in tubular epithelial cells, but instead in fibroblasts that are induced by transforming growth factor β1 (TGFβ1). The authors confirm increased expression of miR-34a in fibroblast cells in culture after incubation with TGFβ1. These cells release miR-34a-containing microvesicles into the medium that, as they show here, can deliver miR-34a into cultured tubular cells. Importantly, the authors demonstrate that microvesicle-mediated delivery of miR-34a induces apoptosis in cultured tubular cells, as well as in mouse kidney, through modulating the expression of the anti-apoptotic factor Bcl-2. This work thus not only highlights microvesicle-mediated delivery as an important means of cell–cell communication, but also provides mechanistic insights into renal fibrosis that could be exploited in future therapeutic strategies.