“We found that cutting the genome with CRISPR-Cas9 induced the activation of … p53,” said Emma Haapaniemi, the lead author of the Karolinska study. That “makes editing much more difficult.”

The flip side of p53 repairing CRISPR edits, or killing cells that accept the edits, is that cells that survive with the edits do so precisely because they have a dysfunctional p53 and therefore lack this fix-it-or-kill-it mechanism.

The reason why that could be a problem is that p53 dysfunction can cause cancer. And not just occasionally. P53 mutations are responsible for nearly half of ovarian cancers; 43 percent of colorectal cancers; 38 percent of lung cancers; nearly one-third of pancreatic, stomach, and liver cancers; and one-quarter of breast cancers, among others.

Yet more trouble for the approach. I think the knowledge about the new type of DNA needs to be expanded before we truly understand this.