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BH3 interacting domain death agonist) is highly dependent on the HIV-1 accessory proteins Tat and Rev, leading to a specific, efficient and rapid killing of productively HIV-1 infected cells [17]

Discussion The discovery of widespread cysteine S-acetylation fundamentally expands our understanding of protein post-translational modifications and reveals a previously hidden layer of cellular regulation

Long-term safety, potential adverse effects, and inconsistent clinical outcomes remain challenges that must be addressed