Our study shows that the hypersensitivity of RECQ1-deficient GBM cells to TMZ supports the notion of RECQ1-PARP1 regulation as a contributor to the resistance of glioblastoma cells to the methylating drug temozolomide and represents a promising target pathway for anticancer therapies that inhibit DNA replication and proliferation of GBM cells. This evidence concerns the gene PARP1 and glioblastoma.