Importantly, the underlying anti-tumor mechanism of DOP was shown to inhibit the transduction of STAT6/PPAR-r signaling by targeting the STAT6 and PPAR-r proteins and the activation of the JAGGED1/NOTCH1 pathway, which may lead to the inhibition of M2 polarization, thereby significantly promoting apoptosis through upregulating Caspase-3, increasing the ratio of Bax/Bcl-2, and inhibiting cell migration by reversing the effects of N-cadherin and vimentin while also increasing the E-cadherin expression. The gene discussed is BCL2; the disease is neoplasm.