Reichold, M. et al. showed that the accumulation of mutant GATM in the mitochondria of the proximal tubule, resulted in mitochondrial enlargement and elongation, eventually leading to renal tubular injury, renal Fanconi syndrome, and later in life, to fibrosis and progressive loss of renal function (Reichold et al., 2018), while another research showed that GATM knockout only caused neurological symptoms due to creatine deficiency but did not caused dysfunctions in renal and renal fibroses (Choe et al., 2013). The gene discussed is GATM; the disease is adult Fanconi syndrome.