For example, Let-7c significantly reduced luciferase activity of Bcl-xL 3′UTR-based reporter, simultaneously reducing Bcl-xL protein levels [111], whereas miR-125b expression induced spontaneous apoptosis in various cell lines derived from lung cancer and sensitized cancer cells to different apoptotic stimuli, probably by suppressing the antiapoptotic molecules Mcl-1 and/or Bcl-w, suggesting that miR-125b downregulation facilitates tumor development [112]. Here, BCL2L1 is linked to lung cancer.