SRC and neoplasm: These conclusions are consistent with the findings of Zhu et al. [92] who suggested that secreted cANGPTL4 binds to integrin β1/β5 and activates focal adhesion kinase (FAK) and ras-related C3 botulinum toxin substrate (Rac1), and then activates Src through PI3K/PKRα and ERK signaling, ultimately promoting tumor growth.