Conversely, exogenous FGF-2 increased the expression of CLDN1, whereas it declined in the presence of neutralizing anti-FGF-2 mAbs and/or pan-FGFR inhibitors, thereby illustrating the functional partnership between CLDN1 and the FGFR pathway and suggesting a novel regulatory role of CLDN1 in GIST resistance to IM. Here, FGF2 is linked to gastrointestinal stromal tumor.