Bim is a pro-apoptotic member of the Bcl-2 family that is induced and contributes to neuron death in response to NGF deprivation. Past work has revealed that Bim is downstream of multiple independent transcriptional pathways in neurons including those culminating in activation of the c-Jun, FoxO and Myb transcription factors. This study addresses the issue of whether the three signaling pathways are redundant with respect to Bim induction or whether they act cooperatively. Examination of the proximal Bim promoter reveals binding sites for FoxO, Mybs and, as shown here, c-Jun. We find that mutation of any one of these types of sites abolishes induction of a Bim-promoter driven reporter in response to NGF deprivation. Moreover, down-regulation of either c-Jun, FoxOs or Mybs by shRNAs blocks induction of Bim promoter-reporter activity triggered by withdrawal of NGF. This was the case for reporters driven by either the proximal promoter or a promoter that also includes additional regulatory elements in the first intron of the Bim gene. Such shRNAs also suppressed the induction of endogenous Bim protein. These findings thus indicate that the Bim promoter acts as a coincidence detector that optimally responds to the simultaneous activation of three different pro-apoptotic transcriptional pathways. Such a mechanism provides a “fail-safe” that prevents neurons from dying by accidental activation of any single pathway. It also permits neurons to utilize individual pathways such as JNK signaling for other purposes without risk of demise.