Because Sp1 protects GBM cells from DNA damage induced by oxidative stress [17], and BA attenuated Sp1 expression (Figure 3), we next examined DNA damage marker γH2AX and found that BA treatment resulted in concentration- and time-dependent increases in γH2AX expression in U87MG, A172, P3, and P11 GBM cells (Figure 6C–E). Here, SP1 is linked to glioblastoma.