Akt’s role as a key inhibitor of apoptosis is well documented, however, evidence of its contribution as a mediator of cell death under various circumstances has begun to emerge as well [45], [47]. Our data demonstrates a new mode of necrosis-specific regulation of Akt by RIP1 kinase. Importantly, while it is possible that necroptosis-specific targets of Akt exist, this regulation clearly involves a number of well established Akt targets including mTORC1, and potentially, GSK-3, FoxO1/4, and MDM2. Therefore, it may no longer be safe to assume that activation of Akt universally reflects pro-survival signaling nor that its inhibition will lead to more cell death. It is tempting to speculate that rather than serving a universally pro-survival role, the Akt pathway may function to promote cell fates alternative to apoptosis, ranging from survival to non-apoptotic cell death. The final decision between survival and death may depend on additional, Akt-independent inputs, such as the status of RIP1 kinase, expression of particular oncogenic factors [45] or excessive metabolic stress [47].