Renal Fanconi syndrome and Porphyric crises are also cited in addition to liver and renal damage. Currently, there is no cure for tyrosinemia type 1. Diagnosed individuals need special dietary restriction all throughout life for the amino acids, phenylalanine and tyrosine. Affected individuals may also be treated with a FDA-approved medication called nitisinone. Recommended treatment should begin as early as possible when the condition is diagnosed. Bacterial inhibition assay, such as the Guthrie Test, can screen newborns for FAH deficiency in addition to increased phenylalanine levels. Other diagnostic methods include measurements with tandem mass spectrometry fragmentation. Some individuals require a liver transplant if liver disease progresses into advanced development before dietary treatment begins. A complete FAH genotype has been previously established. All possible bands show two deleterious mutations. The effect of these mutations for the majority of the abnormalities on the FAH mRNA have been analysed. The identification of the gene defects on both alleles enables an initial genotype-phenotype analysis for chronic, subacute and acute HT 1 patients. The FAH gene is located on the chromosome 15q25.1 region and contains 14 exons. It encodes a protein that is 46kDa in height. Multiple isoforms of the protein have been discovered that arose from alternative splicing. The gene is mainly expressed in the liver and the kidney.