Interest has been growing in the role of activin A in both acute and chronic kidney disease. The role of other activins, however, remains relatively unexplored. In a recent issue of the Journal of Pathology, an elegant study by Sun et al. identified upregulation of INHBB, the subunit of activin B, in three different models of kidney fibrosis, as well as in human kidneys with fibrosis. This increase was shown to be mediated by upregulation of the transcription factor Sox9. Using overexpression and inhibition strategies, the importance of INHBB to kidney interstitial fibroblast activation and kidney fibrosis was clearly shown. Importantly, INHBB and Sox9 are not appreciably expressed in normal tissue. These studies lay important groundwork for the further investigation of activin B targeting as a potential therapeutic approach to attenuate kidney fibrosis.

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