Li et al. (2011) reported that Insulin-like growth factor-I (IGF1) regulated the expression of the VEGF ligand to facilitate angiogenesis and lymphangiogenesis in GC cell lines, and blocking IGF1 could enhance the effectiveness of bevacizumab. High glucose conditions were shown to promote GC cell proliferation and reduce susceptibility to chemotherapy (Zhao et al., 2015). In addition, serotonin-induced signaling pathways promoted tumor progression (Sarrouilhe & Mesnil, 2019). This evidence concerns the gene IGF1 and neoplasm.