MMR-deficient CRC tumours and cell lines frequently tend to accumulate mutations within microsatellite repeats of genes implicated in DSB repair pathway (eg, MRE11 and RAD50) (Giannini et al, 2002; Koh et al, 2005), suggesting an enhanced sensitivity of these tumours to camptothecin analogues. This evidence concerns the gene RAD50 and colorectal carcinoma.