Hutcheson et al. found that 5-HT2B antagonism changed the function and spatial location of Src and physically restricts it to preventing downstream signaling via non-canonical transforming growth factor-β1 (TGF-β1)-p38 MAPK signaling rather than the phosphorylation of Src, that could finally slow down TGF-β1-induced myofibroblast activation of quiescent aortic valve interstitial cells, a differentiation process implicated in calcific aortic valve disease 84. Here, TGFB1 is linked to aortic valve calcification.