Given that the shift to a high MCL-1S/L ratio is associated with increased sensitivity of cancer cells to apoptotic stimuli, specifically through the mitochondrial intrinsic apoptotic pathway [82], the preferential inhibition of the anti-apoptotic MCL-1L isoform, and the concomitant and specific increase in caspase 9 positive cells observed in our study highlights a novel mechanism by which miR-101-3p can induce apoptosis, and points to a possible therapeutic target for oligonucleotide-based therapies. Here, MCL1 is linked to cancer.