Suppressing the recombination of photogenerated charges is one of the most important routes for enhancing the catalytic performance of semiconductor photocatalysts. In addition to the built‐in field produced by semiconductor heterostructures and the photo‐electrocatalysis realized by applying an external electrical potential to photocatalysts assembled on electrodes, other strategies are waiting to be scientifically explored and understood. In this work, a Lorentz force–assisted charge carrier separation enhancement strategy is reported to improve the photocatalytic efficiency by applying a magnetic field to a photocatalytic system. The photocatalytic efficiency can be improved by 26% just by placing a permanent magnet beneath the normal photocatalytic system without any additional power supply. The mechanism by which the Lorentz force acts oppositely on the photogenerated electrons and holes is introduced, resulting in the suppression of the photoinduced charge recombination. This work provides insights into the specific role of the Lorentz force in suppressing the recombination of electron–hole pairs in their initial photogenerated states. This suppression would increase the population of charge carriers that would subsequently be transported in the semiconductor. It is believed that this strategy based on magnetic effects will initiate a new way of thinking about photoinduced charge separation.

Glioblastoma (GBM) is one of the most fatal central nervous system tumors and lacks effective or sufficient therapies. Ferroptosis is a newly discovered method of programmed cell death and opens a new direction for GBM treatment. However, poor blood–brain barrier (BBB) penetration, reduced tumor targeting ability, and potential compensatory mechanisms hinder the effectiveness of ferroptosis agents during GBM treatment. Here, a novel composite therapeutic platform combining the magnetic targeting features and drug delivery properties of magnetic nanoparticles with the BBB penetration abilities and siRNA encapsulation properties of engineered exosomes for GBM therapy is presented. This platform can be enriched in the brain under local magnetic localization and angiopep‐2 peptide‐modified engineered exosomes can trigger transcytosis, allowing the particles to cross the BBB and target GBM cells by recognizing the LRP‐1 receptor. Synergistic ferroptosis therapy of GBM is achieved by the combined triple actions of the disintegration of dihydroorotate dehydrogenase and the glutathione peroxidase 4 ferroptosis defense axis with Fe₃O₄ nanoparticle‐mediated Fe²⁺ release. Thus, the present findings show that this system can serve as a promising platform for the treatment of glioblastoma.