The article reviews the mechanisms by which survival factors regulate the PI3K/c-Akt signaling cascade and its role in promoting cell survival. It highlights the importance of PI3K in mediating survival signals downstream of extracellular stimuli, particularly growth factors (GFs). The activation of PI3K leads to the generation of 3′-phosphorylated phosphoinositides, which recruit and activate c-Akt. c-Akt, an atypical protein kinase, is a key regulator of cell survival and can be activated by various upstream kinases, including PDK1 and CaMKK. The activation of c-Akt is both necessary and sufficient for cell survival, as demonstrated by the use of dominant-negative and constitutively active c-Akt alleles. The article also discusses the role of c-Akt in regulating the apoptotic machinery, including the phosphorylation of Bad and caspase 9, and its involvement in oncogenesis. Additionally, it explores the Forkhead family of transcription factors as potential targets of the PI3K/Akt pathway, suggesting that c-Akt may modulate the expression of genes involved in apoptosis.The article reviews the mechanisms by which survival factors regulate the PI3K/c-Akt signaling cascade and its role in promoting cell survival. It highlights the importance of PI3K in mediating survival signals downstream of extracellular stimuli, particularly growth factors (GFs). The activation of PI3K leads to the generation of 3′-phosphorylated phosphoinositides, which recruit and activate c-Akt. c-Akt, an atypical protein kinase, is a key regulator of cell survival and can be activated by various upstream kinases, including PDK1 and CaMKK. The activation of c-Akt is both necessary and sufficient for cell survival, as demonstrated by the use of dominant-negative and constitutively active c-Akt alleles. The article also discusses the role of c-Akt in regulating the apoptotic machinery, including the phosphorylation of Bad and caspase 9, and its involvement in oncogenesis. Additionally, it explores the Forkhead family of transcription factors as potential targets of the PI3K/Akt pathway, suggesting that c-Akt may modulate the expression of genes involved in apoptosis.