Although the biological mechanism of docetaxel-induced tumor cell death is not fully understood, current knowledge indicates that docetaxel first causes the stabilization of microtubulins by binding to beta-tubulins, thereby resulting in the activation of caspase-dependent apoptosis with consequent cleavage of PARP via mitochondrial pathways in lung, prostate, and ovarian cancers and melanoma cells [28–31]. This evidence concerns the gene TUBB and ovarian carcinoma.