MMP3, as a matrix metalloproteinase, mediates extracellular matrix degradation and induces mitochondrial membrane potential collapse through the PI3K/AKT/mTOR signaling pathway [55]; its overexpression can directly cleave mitochondrial membrane proteins (such as CypD) or promote Ca2+ overload by inhibiting apoptosis, leading to the disruption of MPTP stability, which is significantly associated with CC invasion and poor prognosis [56, 57]. Here, AKT1 is linked to cholangiocarcinoma.