Our hAd-CM model, albeit simple and limited to only hAd-secreted factors, revealed that hAd-CM-promoted radioresistance and aggressiveness of TNBC were dampened when SERPINE1 in both hAd and cancer cells were depleted genetically or pharmacologically (Fig. 5), suggesting that both the adipocyte-secreted and the cancer cell-autonomous SERPINE1 were important to contribute to the aggressive phenotypes. The gene discussed is SERPINE1; the disease is cancer.