The siGmnn-6 construct yields higher knockdown of Gmnn compared to siGmnn-2, suggesting that the extent of Gmnn loss may affect the nature and extent of DNA damage that occurs upon Gmnn knockdown in medulloblastoma cells, with the siGmnn-2 construct predominantly triggering replication stress leading to ATR/Chk1 activation, while more effective knockdown with siGmnn-6 resulted both in higher levels of replicative stress and induction of double strand DNA breaks, activating both pChk1 and pChk2. This evidence concerns the gene ATR and medulloblastoma.