RAD51 and inflammatory bowel disease: Using samples from inflammatory bowel disease (IBD) patients, who are more prone to develop colitis-associated colorectal cancer and have an important neutrophil infiltrate in the intestinal mucosa, they demonstrated that neutrophil-derived EVs containing miR-23a and miR-155 inhibited Homologous Recombination (HR) repair by targeting the main HR regulators RAD51 while promoting non-homologous DNA end joining (NHEJ), ultimately leading to the formation of highly mutagenic DNA Double-Strand Breaks (DSBs) (127).