SOD2 and gestational trophoblastic neoplasm: This concept was supported by previous reports on the improvement of GTN side effects by a mitochondria-targeted antioxidant (mitoQ) [30], by aggravation of GTN toxicity by partial deficiency in the mitochondrial superoxide dismutase (Mn-SOD) [28], and by interference of blockers of the mitochondrial pores (cyclosporine A and glibenclamide) with the crosstalk between cytosolic and mitochondrial sources of RONS [69].