AKT1 and neoplasm: The hyaluronan produced by tumor cells can interact with TLR-4 receptors on neutrophils and induce long-lived neutrophils, which further promotes contact-dependent cancer cell motility; however, this can be blocked by inhibiting the activation of PI3K/Akt signaling in neutrophils, since PI3K/Akt signaling has been implicated in regulating the proinflammatory cytokine expression, thus presenting a potential therapeutic target [49].