BIML is one of several splice variants of BIM, a proapoptotic protein belonging to the BH-3 domain-only subgroup of Bcl-2 family members. BCL-2 family members form hetero- or homodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. BIML is thought to promote apoptosis by binding and inhibiting the activity of anti-apoptotic Bcl-2 family members, thereby inducing the release of cytochrome c from mitochondria. BIML is normally sequestered in an inactive conformation from anti-apoptotic Bcl-2 family members through binding to the microtubule-associated dynein motor complex. Certain apoptotic stimuli release BIML from microtubules to neutralize anti-apoptotic Bcl-2 family members, allowing for the initiation of apoptosis.