This inhibition hampered epithelial‐to‐mesenchymal transition and increased survival rates in mouse models.[134] Conversely, in breast cancer cells, cAMP promoted TGFβ/Smad3‐mediated gene expression by upregulating TGF‐βR1.[135] Although the correlation between cAMP and TGF‐β1/Smad3 signaling pathway is well established, we are unaware of any studies exploring the potential modulatory effects of H4R on the cAMP/TGF‐β1/Smad3 signaling pathway. The gene discussed is TGFBR1; the disease is breast carcinoma.