Such specificity for the addition of a thymine 3′ to the ERG cognate sequence may presumably limit their inhibition efficiency on ERG protein binding to all potential ERG cognate sequence (with a cytosine, an adenine or a guanine steigth at the 3′-end) but this offers the opportunity to modulate ERG inhibition to some ERG-driven genes, assuming that the crucial ERG-driven genes associated with cancer development are well characterize and are controlled through a ERG cognate sequence followed by a thymine in its 3′-end. The gene discussed is ERG; the disease is cancer.