14‐3‐3ζ proteins have also been proved to intercommunicate with other survival‐promoting proteins such as phosphoinositide 3‐kinase (PI3K) and growth factor receptors.14 However, the mechanism of those interactions, especially related to tumor progression, is not well understood.15, 16 In this study, we demonstrate that 14‐3‐3ζ overexpression is related to the malignancy of gliomas, and Snail is up‐regulated by 14‐3‐3ζ through activating PI3K/AKT signaling. The gene discussed is SNAI1; the disease is neoplasm.