AKT1 and neoplasm: As a result, our data illustrated that tumor-derived EVs could augment KCNQ1OT1 expression and reduce miR-556-3p expression by transferring c-Myc to GC cells to upregulate CLIC1 and activate the PI3K/AKT pathway, so as to enhance GC cell proliferating, migrating, and invasive potential.