Abstract
Mothers against decapentaplegic homolog (SMAD) proteins exert a wide spectrum of transcriptional effects in different cell types and tissues in response to transforming growth factor-β (TGF-β). A recent study demonstrates what is thought to be the first distinct cytoplasmic function for SMAD2 in modulating mitochondrial dynamics and hence reveals new pathophysiological implications for TGF-β signaling.