Further exploration of the signaling pathways and related targets of serine metabolism reprogramming from a mechanistic perspective reveals that KRAS-driven PHGDH expression mutations alter the reprogramming of serine metabolism in cholangiocarcinoma (CCA), activating the tumor serine-glycine pathway and increasing glucose flux into serine synthesis, ultimately enhancing CCA cell viability [55]. Here, PHGDH is linked to neoplasm.