BCLAF1 was originally identified as a protein that interacts with antiapoptotic members of the Bcl2 family. Initial studies indicated a role for this protein as an inducer of apoptosis and repressor of transcription. Subsequent studies have shown that BCLAF1 plays criticals roles in a wide range of processes that are not normally associated with actions of Bcl2 family members, including lung development, T-cell activation, and control of the lytic infection program of Kaposi's sarcoma-associated herpesvirus. Here, we provide an overview of findings from past studies that both support and challenge the role of BCLAF1 in cell death and transcriptional control. We also present recent findings from our laboratory and others indicating a role for BCLAF1 in post-transcriptional processes that impact mRNA metabolism, instead of a direct role for this protein in apoptosis or transcription.