In human papillary thyroid carcinoma cells, shikonin inhibited cell proliferation and led to apoptosis in a dose- and time-dependent manner through mitochondrial pathways, as reflected in enhanced Bax levels, reduced antiapoptotic protein Bcl-2 levels, decreased mitochondrial membrane potential, and activated caspase-3 enzymatic activity [32]. The gene discussed is BAX; the disease is differentiated thyroid carcinoma.