More recently it was argued that the DNA break leading to mitotic recombination happened during G1, but repair happens after replication.

ATR is involved in arresting the cell cycle in response to DNA double-stranded breaks.

Further, these studies indicate that rereplication can result in an increase in aneuploidy, chromosomal fusions, and DNA breaks.

DNA breaks can increase the likelihood of developing cancer (if the damage is to a tumor suppressor gene)

DNA breaks are the most lethal damage for cells, as one single double-strand break if unrepaired is sufficient to lead to cell death.

The RAG proteins remain at these junctions until other enzymes repair the DNA breaks.

With 1q21.1 deletion syndrome a disturbance occurs, which leads to increased DNA breaks.

DNA ds breaks play a key role in homologous recombination.

This process, homologous recombination, completes the repair of the double-stranded DNA break.

Glutathione seems to play an important role by protecting against benzene-induced DNA breaks and it is being identified as a new biomarker for exposure and effect.