Previous studies from our group and others identified DNAPKcs as a mediator of AR-inducted radioresistance in prostate cancer, and we hypothesized that a similar mechanism may be acting in TNBC.6, 16 DNAPKcs is a serine/threonine kinase involved in non-homologous end joining, the key repair pathway responsible for repair of dsDNA breaks induced by ionizing radiation. This evidence concerns the gene MARK2 and prostate cancer.