Historically, necrotic cell death (characterized by cell swelling, membrane rupture, lysis and inflammation) has largely been thought to be a non-specific/unprogrammed process and thereby void of distinct signaling events and genetic players. Recently, it has become clear that necrosis, like apoptosis, may be highly regulated and involve specific gene programs.  Of clinical importance, cellular necrosis underlies many human disease states such as ischemic injury, neurodegenerative diseases, and other adult onset diseases. The lab has various projects examining genes and pathways that contribute to cellular necrosis with the hope of finding new therapeutic targets to block cell death in disease.