In contrast, at later stages where active TGF-β1 is expected to be abundant at doses within the same range used in our experimental settings [18, 21], the impaired migration observed in all SMAD2/3 conditions concomitantly with the expected α-SMA-dependent increased contractility may collectively increase the spatial confinement of TAFs and ultimately facilitate the long-term interactions with adjacent cancer cells to promote their epigenetic reprogramming [52, 66] (Fig. 6g). Here, TGFB1 is linked to cancer.