TGFB1 and neurofibromatosis type 1: Taking into account the data from several genetic and experimental studies that unveiled the pathophysiological contribution of TGF-β1 signaling in syndromes, such as Camurati-Engelmann [80,81], Loeys-Dietz [82,83], Shprintzen-Goldberg [82,84,85] or Marfan disease [86,87], and their clinical presentations with severe skeletal malformations including altered remodeling, osteoporosis and dystrophic scoliotic deformities, the link between scoliosis or other bone defects in NF1 and induction of TGFβ1-Smad axis is an interesting hypothesis.