However, clock genes are not major effectors in miR-34a-mediated effects on cancer progression, and we suppose that effects mediated by per2 and bmal1 are under control conditions overwhelmed by the effect of other target genes of miR-34a, whose oncogenic capacity (e.g., sirt1 and survivin) is higher than the tumour-suppressive capacity of the above-mentioned clock genes. The gene discussed is BMAL1; the disease is neoplasm.