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Demethylating agents or histone deacetylase (HDAC) inhibitors may overcome epigenetic reppression of BIM transcription, whereas MEK inhibitors (e.g. trametinib) decrease BIM degradation—all leading to increased cellular BIM protein levels and increased activation of BAX. BCL-2/BCL-XL inhibitors (e.g. navitoclax) block the ability for anti-apoptotic BCL-2 family members like BCL-2 and BCL-XL to neutralize BIM.
