In a pair of cell lines derived from the same tumor, CPH-54A and CPH-54B, the more resistant cell line had higher levels of DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and RAD51 recombinase (RAD51), as well as a higher rate of double-strand break repair, suggesting that both non-homologous end joining (NHEJ) and homologous recombination (HR) may be involved [179]. This evidence concerns the gene RAD51 and neoplasm.