One of the biggest challenges for activated PPARγ-based therapeutic strategies is that these molecules have strong efficacy in inducing autophagy through the upregulation of the hypoxia-inducible factor 1 (HIF1α) [36], in triggering apoptosis [21], and in inhibiting the migration and invasion process by upregulating the expression of E-cadherin [22] in triple-negative breast cancer cells. The gene discussed is PPARG; the disease is triple-negative breast carcinoma.