McGuire et al. (1989) found that a mutation in nucleotide 209, which changes codon 70 from GAT to GGT, was the abnormality in all 5 atypical cholinesterase families examined. The mutation caused the loss of a Sau3A1 restriction site. The gene change results in a substitution of glycine for aspartic acid as amino acid 70. This is an acidic to neutral amino acid change which accounts for the reduced affinity of atypical cholinesterase for choline esters. Aspartic acid must be an important component of the anionic site. Atypical BCHE, the classic deficiency variant described by Kalow (1962) , Kalow and Gunn (1959) , Kalow and Staron (1957) , has a homozygote frequency of about 1:3,000 in white North Americans. In the nomenclature system of La Du et al. (1991) , this allelic variant is referred to as CHE*70G.
In the United Kingdom , there were no restrictions on paternity tests until the Human Tissue Act 2004 came into force in September 2006. Section 45 states that it is an offence to possess without appropriate consent any human bodily material with the intent of analysing its DNA. Legally declared fathers have access to paternity-testing services under the new regulations, provided the putative parental DNA being tested is their own. Tests are sometimes ordered by courts when proof of paternity is required. In the UK, the Ministry of Justice accredits bodies that can conduct this testing. The Department of Health produced a voluntary code of practice on genetic paternity testing in 2001. This document is currently under review, and responsibility for it has been transferred to the Human Tissue Authority .