These AIF-deficient mouse models are important for fixing complex I deficiencies. The identification of AIF-interacting proteins in the inner mitochondrial membrane and intermembrane space will help researchers identify the mechanism of the signalling pathway that monitors the function of AIF in the mitochondria.
Mice lacking AIF have proven valuable for studying complex I deficiency.  Identifying proteins interacting with AIF within the mitochondria's inner and outer membranes is crucial to understanding how AIF regulates mitochondrial function through a signaling pathway.