The intrinsic apoptosis pathway, regulated by the BCL‐2 protein family, is essential for embryonic development. Using mice lacking all known apoptosis effectors, BAX, BAK and BOK, we have previously defined the processes during development that require apoptosis. Rare Bok−/−Bax−/−Bak−/− triple knockout (TKO) mice developed to adulthood and several tissues that were thought to require apoptosis during development appeared normal. This raises the question if all apoptosis had been abolished in the TKO mice or if other BCL‐2 family members could act as effectors of apoptosis. Here, we investigated the role of BID, generally considered to link the extrinsic and intrinsic apoptosis pathways, acting as a BH3‐only protein initiating apoptosis upstream of BAX and BAK. We found that Bok−/−Bax−/− Bak−/−Bid−/− quadruple knockout (QKO) mice have additional developmental anomalies compared to TKO mice, consistent with a role of BID, not only upstream but also in parallel to BAX, BAK and BOK. Mitochondrial experiments identified a small cytochrome c‐releasing activity of full‐length BID. Collectively, these findings suggest a new effector role for BID in the intrinsic apoptosis pathway. Synopsis The combined loss of the apoptosis effectors BAX, BAK and BOK abrogates detectable developmental apoptosis, but some tissues known to undergo apoptosis develop normally. Here, loss of BID, previously considered to only act as a BH3‐only protein upstream of BAX and BAK, is found to increase developmental defects in mice also lacking BAX, BAK and BOK, suggesting that it may promote apoptosis in a multi‐BH domain pro‐apoptotic protein‐like manner. BID deletion in a background of BAX/BAK/BOK knockout (quadruple KO) causes additional birth defects, implying BID action in parallel and not just upstream. In vitro, full‐length BID can induce some cytochrome c release from mitochondria, suggesting that BID, like BAX and BAK, may form pores in the outer mitochondrial membrane. The pro‐apoptotic protein BID affects embryonic development independent of its known role as an upstream regulator of Bax, Bak and Bok, likely by directly promoting mitochondrial cytochrome c release.