The activation of either the ERK1–ERK2 or the PI3K signalling pathways by ERs results in the decreased expression of BAD and in the upregulation of BCL 2 (REFS 89–92). ER activation also induces the transcrip¬tion of BCL2 and another anti apoptotic gene, survivin, through signal transducer and activator of transcrip¬tion 3 (STAT3), a transcription factor that mediates neuroprotective actions of the hormone in experimental cerebral ischaemia93–95. In addition, some members of the BCL 2 family, such as BCL W and BIM are regu¬lated by oestradiol through the inhibition of JNK86. Thus, several redundant mechanisms are elicited by oestradiol to control apoptosis in the brain.