MAX and neoplasm: Recently, some studies have exploited aptamers as ligands in aptamer‐based PROTAC.[17] Among them, TNA (threose nucleic acid) aptamers targeting the c‐Myc/Max dimer are conjugated to E‐box (double‐stranded DNA), and the conjugates act as a ligand in PROTAC (TNA‐E box‐pomalidomide, TEP) to degrade c‐Myc/Max dimer.[18] However, single TEP is ineffective in tumor suppression in mice.