We found that the drug exerted its activity within the tumour cells as shown by (a) the presence of acetyl-H3 and γ-H2AX (the latter denoting drug-induced caspase activation and DNA damages) and (b) the marked decrease, as compared to untreated mice, in the amount of tumour cells positively-stained with MIB-1 (against the nuclear marker Ki-67 associated with cell proliferation [32–34]. Here, MIB1 is linked to neoplasm.