Although PDS can bind to many G4s without selectivity, it is thought to constitute a suitable model for such a proof‐of‐concept study,[30] as exemplified by the use of PDS to reduce SRC proto‐oncogene expression in human breast cancer cells and to validated SRC‐G4 as a druggable target.[31] We first measured the half‐maximal inhibitory concentration (IC50) values of PDS to Hela, A431, and A549 cells to be 109.2, 204.4, and 203.5 μm, respectively (Figure S28A, Supporting Information). Here, SRC is linked to breast carcinoma.