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Background: Bad is a pro-apoptotic member of the Bcl-2 family. Bad will bind preferentially Bcl-xL over Bcl-2 through its partial (9-16 a.a) BH3 domain. Additionally, Bad can reverse the death repressor activity of Bcl-xL but not of Bcl-2. Upon dephosphorylation, activated Bad translocates to the mitochondria and displace Bcl-2 from tBid sequestration to initiate mitochondrial dysfunction. The switching on/off of its phosphorylation by growth/survival factors regulates Bad activity.