The accumulation of mutations in the human genome is at the origin of cancers, as well as the development of resistance to treatments. The Cyclin E and Myc genes are active in the control of cell division. When they mutate in response to a carcinogen, these genes induce cells to replicate their DNA prematurely during the cell cycle. This abnormal cell division causes a tumor to develop. Why is this the case? Biologists from the University of Geneva (UNIGE), Switzerland, show that precocious entry of the genome into the replication phase leads to molecular collisions occurring on the DNA and induces new mutations. These results, published in the journal Nature, could be used to develop new therapeutic approaches.