In contrast, Kratschmer et al. provided a direct conjugation strategy, by generating small-molecule aptamer–toxin conjugates of auristatin, monomethyl auristatin E (MMAE), and monomethyl auristatin F (MMAF), and confirmed the improved cytotoxicity of MMAE and MMAF conjugated to an anti-transferrin receptor aptamer and an anti-EGFR aptamer in three different human pancreatic cancer cell lines [107]. This evidence concerns the gene EGFR and familial pancreatic carcinoma.