A consistent observation was that the combined silencing of F2RL1 and TGFBRI had no additive or synergistic effect on TGF-β1-induced Smad2/3 activation over that of silencing TGFBRI alone providing indirect evidence that PAR2 and ALK5 act together as a functional unit and in the same pathway during tumour progression as has recently been suggested for PAR2 and PAR1 [40]. The gene discussed is TGFB1; the disease is neoplasm.