Numerous studies have proven the anti-tumor effects of PCK1. It has been reported that the viability of HepG2 cells is raised through knocking down PCK1, while increasing the expression of PCK1 activates adenosine 5′-monophosphate-activated protein kinase (AMPK) and c-Jun pathways, blocks gluconeogenesis, and promotes TCA cataplerosis, leading to cell cycle arrest and tumor cells death [32, 33]. Here, JUN is linked to neoplasm.