In fact, the ligand showed to markedly inhibit the growth of melanoma cells through its capability to efficiently interact with telomeric G4s [17] and it displayed fairly good binding properties for G4 structures forming within the promoter regions of MYC and KIT (Supplementary Table S2, [31]) as well as of BCL2 [31], other than RET. Nonetheless, its capability to inhibit the expression levels of each oncogene in living cells was not observed straightforwardly, being rather dependent on the cell context [31]. This evidence concerns the gene KIT and melanoma.