We boldly speculate that these findings may be linked to an earlier opinion that increased AS1411 could cause hyperstimulation of micropinocytosis in tumor cells and provoke enhanced cellular uptake 57, thus facilitating AS1411-SL1 chimeras-induced intracellular degradation of c-MET via a ubiquitin-proteasome pathway, rather than simply modulating p-c-MET level on the tumor cell surface. Here, MET is linked to neoplasm.