Several cDNA plasmids expressing FGFR protein variants partially rescued the induction of cell cycle arrest and apoptosis induced by aprotoxin A, and phosphorylation of STAT3, a downstream target of FGFR, was inhibited by aprotoxin A. An inverse correlation of FGFR expression with aprotoxin A sensitivity in a panel of cancer cell lines was also observed, suggesting that a highly expressed FGFR pathway is one mechanism of resistance to aprotoxin A in cancer cell lines. This evidence concerns the gene STAT3 and cancer.