Finally, to explore the therapeutic potential of targeting the KYNU–HDAC6–complement axis, we investigated the effects of the BET inhibitor apabetalone, which has shown promise in GBM by modulating tumor-intrinsic pathways, enhancing temozolomide sensitivity particularly in MGMT-unmethylated cases, and overcoming resistance mechanisms when used in combination therapies [15,16]. The gene discussed is MGMT; the disease is glioblastoma.