DEX-induced activation of the circadian clock was assumedto be responsible for slowing tumor cell proliferation and upregulationof rhythmic clock genes, including Per1, Per2, Cry1, and Nr1d1, along with the protein level of BMAL1.To further confirm that the inhibitory effect of DEX on tumor growthwas due to activation of the clock, the BMAL1 genewas knocked down; as expected, the relative tumor volume could nolonger be suppressed and the rhythmicity of most BMAL1 target geneswas disrupted. The gene discussed is CLOCK; the disease is neoplasm.