Studies12, 54 have found that NEO1 was upregulated in GC patients and cells and NTN4 overexpression mediated NEO1‐induced decreased phosphorylation of Stat3, ERK, AKT and p38 and enhanced GC cell proliferation and invasion, suggesting that NTN4 may be involved in GC development through multiple oncogenic pathways (JAK/STAT, PI3K/AKT and ERK/MAPK). This evidence concerns the gene SOAT1 and gastric cancer.