To rule out the possibility that higher TGFβ response observed in DMD myotubes was due the higher basal levels of pSMAD2/3 (Fig. 2c–e), we pre-treated control and DMD hiPSC-derived myotubes with the SB-431542 ALK5 (TGFβRI) inhibitor 24 h prior to the exposure to TGFβ (Fig. 3e). Here, TGFB1 is linked to Duchenne muscular dystrophy.