Autophagy promotes tumor cell survival and restricts necrosis, inflammation, and tumorigenesis. Defective apoptosis in epithelial cells leads to tumorigenesis, but the role of autophagy in this process is unclear. In apoptosis-defective cells, inhibition of autophagy by AKT activation or beclin1 disruption increases sensitivity to metabolic stress by blocking an autophagy-dependent survival pathway. While autophagy helps buffer metabolic stress, the combined impairment of apoptosis and autophagy promotes necrotic cell death in vitro and in vivo. Inhibiting autophagy under nutrient limitation can restore cell death to apoptosis-refractory tumors, but this necrosis is associated with inflammation and accelerated tumor growth. Thus, autophagy may function in tumor suppression by mitigating metabolic stress and, in concert with apoptosis, by preventing death by necrosis. Apoptosis is a well-defined process of cellular dismantling that leads to cell corpses engulfed by phagocytosis. BCL-2 family proteins regulate apoptosis, with BCL-2 being antiapoptotic and BAX/BAK being proapoptotic. Deficiency in BAX/BAK or expression of BCL-2 blocks apoptosis, promoting tumorigenesis. Autophagy, a catabolic process, allows cells to self-digest intracellular organelles, but can also lead to cell death. Autophagy is evolutionarily conserved and genetically controlled, and its impairment can lead to tumorigenesis. Necrosis, a form of cell death associated with physical insults and ATP depletion, is linked to poor prognosis in cancer. However, necrosis is not under genetic control, and its propensity is influenced by factors like poly-ADP-ribose polymerase. The study shows that autophagy promotes cell survival in solid tumors, and the coordinated inactivation of apoptosis and autophagy promotes necrosis and tumor progression associated with inflammation. AKT promotes tumor growth in both wild-type and apoptosis-defective genetic backgrounds. In apoptosis-defective cells, AKT promotes necrosis in response to metabolic stress. AKT activation in apoptosis-defective cells stimulates necrosis in response to metabolic stress in vitro. AKT inhibits autophagy-mediated survival in ischemia, potentially eliminating a survival mechanism resulting in necrosis. Knockdown of autophagy promotes sensitivity to metabolic stress. Autophagy enables survival of iBMK cells to metabolic stress when apoptosis is inactivated. Necrosis is distinct from apoptosis and is a less efficient means of cell death. Autophagy in tumors localizes to the center prior to acquisition of a blood supply. Beclin1 haploinsufficiency impairs survival in ischemia in an apoptosis-defective background and promotes epithelial tumorigenesis. Autophagy deficiency promotes tumor growth and necrosis. Tumor necrosis stimulates an inflammatory response, which may impact tumor growth. The study highlights theAutophagy promotes tumor cell survival and restricts necrosis, inflammation, and tumorigenesis. Defective apoptosis in epithelial cells leads to tumorigenesis, but the role of autophagy in this process is unclear. In apoptosis-defective cells, inhibition of autophagy by AKT activation or beclin1 disruption increases sensitivity to metabolic stress by blocking an autophagy-dependent survival pathway. While autophagy helps buffer metabolic stress, the combined impairment of apoptosis and autophagy promotes necrotic cell death in vitro and in vivo. Inhibiting autophagy under nutrient limitation can restore cell death to apoptosis-refractory tumors, but this necrosis is associated with inflammation and accelerated tumor growth. Thus, autophagy may function in tumor suppression by mitigating metabolic stress and, in concert with apoptosis, by preventing death by necrosis. Apoptosis is a well-defined process of cellular dismantling that leads to cell corpses engulfed by phagocytosis. BCL-2 family proteins regulate apoptosis, with BCL-2 being antiapoptotic and BAX/BAK being proapoptotic. Deficiency in BAX/BAK or expression of BCL-2 blocks apoptosis, promoting tumorigenesis. Autophagy, a catabolic process, allows cells to self-digest intracellular organelles, but can also lead to cell death. Autophagy is evolutionarily conserved and genetically controlled, and its impairment can lead to tumorigenesis. Necrosis, a form of cell death associated with physical insults and ATP depletion, is linked to poor prognosis in cancer. However, necrosis is not under genetic control, and its propensity is influenced by factors like poly-ADP-ribose polymerase. The study shows that autophagy promotes cell survival in solid tumors, and the coordinated inactivation of apoptosis and autophagy promotes necrosis and tumor progression associated with inflammation. AKT promotes tumor growth in both wild-type and apoptosis-defective genetic backgrounds. In apoptosis-defective cells, AKT promotes necrosis in response to metabolic stress. AKT activation in apoptosis-defective cells stimulates necrosis in response to metabolic stress in vitro. AKT inhibits autophagy-mediated survival in ischemia, potentially eliminating a survival mechanism resulting in necrosis. Knockdown of autophagy promotes sensitivity to metabolic stress. Autophagy enables survival of iBMK cells to metabolic stress when apoptosis is inactivated. Necrosis is distinct from apoptosis and is a less efficient means of cell death. Autophagy in tumors localizes to the center prior to acquisition of a blood supply. Beclin1 haploinsufficiency impairs survival in ischemia in an apoptosis-defective background and promotes epithelial tumorigenesis. Autophagy deficiency promotes tumor growth and necrosis. Tumor necrosis stimulates an inflammatory response, which may impact tumor growth. The study highlights the