Based on previous studies, mitochondrial dysfunction may contribute to cholelithiasis through the following mechanisms: Disruption of the TCA cycle leads to an imbalance in the NADH/NAD+ ratio, activating the sterol regulatory element-binding protein (SREBP) pathway and upregulating cholesterol biosynthesis.[35] Impaired branched-chain amino acid degradation induces insulin resistance, which indirectly increases bile cholesterol saturation.[27]. Here, CNBP is linked to Insulin resistance.