Description
While ACSL4-driven ferroptosis was strongly supported, the molecular triggers that tip the balance from protective GPX4 activity to pathological ACSL4-mediated vulnerability remain unclear. This balance point could be a critical therapeutic target.
Source: Debate session sess_SDA-2026-04-02-gap-seaad-v4-20260402065846 (Analysis: SDA-2026-04-02-gap-seaad-v4-20260402065846)