Since tumor cells frequently inactivate the mitochondrial apoptosis pathway by overexpression of antiapoptotic Bcl-2 members (such as Bcl-2, Bcl-xL, or Mcl-1) to acquire therapy resistance—it was remarkable that VDT was proficient to induce apoptosis in Bcl-2 overexpressing Jurkat cells or in Bax-/Bak-deficient DG75 cells. Here, MCL1 is linked to neoplasm.