The aim of our study was to reveal if transcriptionally active p73 (TAp73), a homolog of the well-known tumor suppressor p53, inhibits tumor progression through promoting canonical TGF-β/Smad signaling and by preventing non-canonical extracellular signal-regulated kinases (ERK)1/2-mediated TGF-β signaling. Here, TP53 is linked to neoplasm.