Although SB431542 significantly inhibited the induction of COL1A1 and αSMA in organoids in response to TGFβ treatment (Fig. 5I), no significant reversal was observed on hallmarks of fibrosis induced by engraftment of patient cells, suggesting that additional profibrotic signals derive from the myelofibrosis clone beyond TGFβ or an inability to reverse fibrosis once established. The gene discussed is ACTA1; the disease is myelofibrosis.