The suppression of mitotic phosphorylation/degradation of Mcl1 and phosphorylation of Bcl-xL in DR3 knockdown cells suggests DR3 is epistatic in the apoptotic pathway, and a crosstalk occurs when caspase-8 activation leads to cleavage of Bid, a Bcl-2-interacting protein that activates the mitochondrial pathway.45 We now hypothesize that anti-mitotics stimulate autocrine secretion of a TNF family member of death ligand TL1A, which is subsequently used as the extrinsic death signal by cancer cells. The gene discussed is MCL1; the disease is cancer.