Man, that's a huge milestone considering the fears with gene editing directly in patients has been poor efficiency and accidentally making the target cells cancerous. I'd still be cautious on the cancer front, but this makes for an amazing breakthrough for the CART field! Also TALENs may be "older", but they general have better target specificity than CRISPR, the downside being that the targeting is specified by the protein sequence (which is a bit harder to design / screen) rather than RNA (where designing is a matter of writing a sequence complementary to the target). It's pretty much expected that the first wave of gene therapies will all be TALENs / ZFNs.But the first versions of their experimental therapies require extracting the T cells from the patient, shipping them to a manufacturing plant where they can be altered, then sending them back and putting them back into the patient, something that will be logistically challenging and costly for thousands of patients. Cellectis’s therapy is meant to work for any patient with a particular type of leukemia.
But to make its treatment “universal,” Cellectis then takes another step using another new technology that is generating huge excitement — genome editing. This refers to using molecular scissors to make precise changes to DNA, just as one might edit a word in a document. The genome editing technique that has gotten the most attention is known as Crispr-Cas9, though Cellectis used an older approach known as Talens.
Better target specificity in the best case scenario, maybe, but given the improvements in simplicity I would've thought CRISPR/Cas9 (or, now, CRISPR/Cpf1) still has the bigger fanbase. The length of the recognition sequence creates insignificant nonspecificity, something on the order of 10^-7 chance of repeat events in the human genome, if my professor did the calculations right. They did get that Zuckerberg rockstar award too...
Well, CRISPR is more flexible in targeting a new sequence, but the current crop of therapies already have screened TALEN / ZFN mutants that target their gene of interest, so that advantage is somewhat moot. The non-specificity is I think a much bigger problem than you expect due to the fact that Cas9 can cut sites where it has at least a partial match of its guide RNA to the DNA. Even if there is only one exact match to the gRNA in a genome, there are still millions of PAMs where Cas9 will at least transiently bind, and a partial match in the early sequence can cause the enzyme to stick around long enough to cleave the DNA in a non-trivial fraction of the time. Keep in mind that Cas9 was primarily evolved to target viral genomes, which are generally pretty small (well less than 1 Mb) in a background of bacteria genomes (~ 2 Mb, say, for S. pyogenes). In contrast, the human genome is about 3,000 Mb in size, which means you need 3 orders of magnitude more specificity than the protein was evolved for. Not impossible, but it means you need a bit of tweaking to the system. There are several tricks people have come up with to reduce this off-target cleavage, but it's still not a solved problem to the point that you would feel safe putting the system in a life human body. Add to that the on-going patent dispute over Cas9 and you have a pretty good incentive to wait it out while academic researchers iron out the bugs with the technology.