The evidence suggests that gastric cancer cells stimulate lymphangiogenesis through the secretion of VEGFC, a process typically facilitated by other regulatory factors, such as transforming growth factor β1 (TGFβ1) and MACC1, in the TME.182,183 Our recent study reported that CRIP1 reshaped the gastric TME to increase the lymphangiogenesis and lymphatic vessel permeability by increasing the amount of secreted VEGFC and CCL5.184 Additionally, tumor-associated lymphangiogenesis and lymph node metastasis is influenced by metabolic factors. This evidence concerns the gene VEGFC and neoplasm.