Interestingly, genetically modified cells harboring STAG2 mutations proliferated slightly more slowly than isogenic parental cells with wild-type STAG2 –a result which was then confirmed by measuring the proliferation of several additional isogenic sets of GBM cells in which the endogenous mutant allele of STAG2 had been corrected by human somatic cell gene targeting. The gene discussed is STAG2; the disease is glioblastoma.