In summary, this work shows that: G4-DNA near the transcription start sites of HRAS behaves as a transcription repressor; MAZ and Sp1 bind to G-elements that can fold into quadruplex forming sequences; transcription is activated by MAZ and Sp1; MAZ destabilized the HRAS G-quadruplexes; G4-decoys mimicking the HRAS quadruplexes behave as decoy molecules against MAZ and cause a potent antiproliferative effect in T24 bladder cancer cells bearing mutant HRAS; the decoy strategy could provide a new therapeutic approach to treat bladder cancer. Here, MAZ is linked to urinary bladder cancer.