Sometani et al. have shown that TGF-β1 administered to cortical neurons of the rat increases BDNF and TrkB expression, suggesting that BDNF may require TGF-β1 in order to carry out its neurotrophic effects.45 Both BDNF and TGF-β1 also appear to regulate the Gadd45 family of enzymes, which have been implicated in psychiatric diseases.46 Although it is unclear in what capacity BDNF and TGF-β1 exert their influence in persistent disability and pain in humans, their association is at least biologically plausible. This evidence concerns the gene TGFB1 and psychiatric disorder.