MFN2 and injury: In contrast to its pro-apoptotic effect observed in vitro, PT-MFN2-CKO enhances the Ras-ERK pathway to promote kidney cell proliferation and thus accelerate the repair process after kidney injury [600], this suggests that the detrimental effects of MFN2 knockdown-mediated inhibition of mitochondrial fusion are counteracted or outweighed by the ERK signaling pathway, which manifests as increased proliferation of kidney cells.