Autocrine VEGF–VEGFR2 signaling in gastric cancer cells stimulates proliferation via a PLCγ–ERK1/2-dependent mechanism, and selective inhibition with apatinib suppresses tumor growth in vitro and in vivo, but predominantly in VEGFR2-high cells, underscoring the functional relevance of autocrine signaling and the potential for biomarker-driven therapy [42]. Here, VEGFA is linked to neoplasm.