Nintedanib potently inhibited the phosphorylation of KIT, such as Y703, Y719 and Y823, and downstream mediators, such as AKT and STAT3, which was also observed in cell lines with high expression RTK drug targets [35], in GIST‐T1 and GIST‐882 (imatinib sensitive) cells. This evidence concerns the gene STAT3 and gastrointestinal stromal tumor.