Trait selection and enhancement in embryos raises moral issues involving both individuals and society. First, does selecting for particular traits pose health risks that would not have existed otherwise? The safety of the procedures used for preimplantation genetic diagnosis is currently under investigation, and because this is a relatively new form of reproductive technology, there is by nature a lack of long-term data and adequate numbers of research subjects. Still, one safety concern often raised involves the fact that most genes have more than one effect. For example, in the late 1990s, scientists discovered a gene that is linked to memory (Tang et al., 1999). Modifying this gene in mice greatly improved learning and memory, but it also caused increased sensitivity to pain (Wei et al., 2001), which is obviously not a desirable trait. A recent study published in the journal Nature Methods has raised concerns that testing CRISPR in humans may be premature, even with CRISPR-Cas9.4 By modifying an enzyme called Cas9, the gene-editing capabilities are significantly improved, in some cases reducing the error rate to "undetectable levels." As precise as the technology is, however, it's not perfect, and it may accidently hit other parts of the genome. This flaw isn't unheard of, and it's been tested for before, typically using a computer algorithm to predict where such off-target mutations are likely to occur, then searching those areas to see if such mutations did, in fact, occur. The new study used a different method to search for unintended mutations, based on a separate study that used CRISPR-Cas9 to restore sight in blind mice by correcting a genetic mutation. Someday, researchers may be able to use gene editing to repair the flawed gene in cells that causes diseases like Hunter syndrome. However, that's not the goal of the trial, sponsored by Sangamo Therapeutics, a biotech company based in Richmond, California. Instead, the company inserts a replacement copy of the gene, using gene editing to snip the DNA helix of liver cells in a specific place near the promotor, or on-off switch, for the gene for a protein called albumin. The cells fix the damage by inserting the DNA for the new gene, supplied by the researchers along with the gene editor's DNA scissors, and the gene's activity is then controlled by the powerful albumin promotor. The idea is to turn these modified liver cells into a factory for making the enzyme missing in Hunter syndrome.