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Akt is deactivated and Bcl-2-associated death promoter (BAD) phosphorylation is lost in one pathway due to a stalled survival pathway, whereas Fas cell surface death receptor (FAS) is upregulated through stimulation of c-Jun-N-terminal kinase, which activates caspase-8, phosphorylates Fas-associated protein with death domain (FADD), and truncates BH3-interacting domain death agonist (BID)

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[PubMed: 14677792] (Cross sectional survey of 98 Australian aboriginal people for kava use, finding higher levels of GGT [78 vs 34 U/L] and Alk P [165 vs 109 U/L] in recent users vs non-users, but no differences in ALT [25.5 vs 24 U/L], the abnormalities being reversible and not associated with clinical symptoms)