T cells have a well-described role in renal injury, which leads to the secondary development of renal fibrosis. It has generally been assumed that this fibrotic response is an indirect consequence of T cell-mediated renal injury, rather than T cells' being directly involved in fibrosis. Tapmeier et al. now provide evidence that CD4(+) T cells promote interstitial fibrosis in the obstructed mouse kidney in a mechanism that appears to dissociate myofibroblast accumulation and matrix deposition.