Moreover, the results of our study demonstrate that the use of a low-molecular-weight inhibitor of antiapoptotic Bcl-2 proteins, such as Navitoclax [117], can increase the sensitivity of apoptosis-resistant THP-1 AML cells to chemotherapeutic agents and the cytokine TRAIL—an effector of antitumor immunity—under conditions of a sterile inflammatory response. Here, TNFSF10 is linked to acute myeloid leukemia.