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When released from anti-apoptotic multi-domain BCL-2 family members (BCL-2, BCL-xL, myeloid cell leukemia 1 (MCL-1), BCL-w, and A1), the BH3-only pro-apoptotics are free to activate the pro-apoptotic effectors BCL-2 associated X protein (BAX) and BCL-2 antagonist/killer (BAK)

Additionally, it controls the expression of pro-inflammatory cytokines and immune regulatory processes

Efficient clinical scale gene modification via zinc finger nuclease-targeted disruption of the HIV co-receptor CCR5

Conclusions and future directions Ferroptosis, a distinct form of iron-dependent cell death driven by lipid peroxidation, has emerged as a key pathological mechanism underlying multiple cognitive disorders, including AD, PD and DACI