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Subsequent research confirmed that gp91phox, a key subunit of NOX2, promotes microglial activation, neuroinflammation, and ferroptosis, contributing to cognitive deficits in PD micesuggesting that targeting gp91phox may offer a promising therapeutic strategy (Tian et al., 2024)

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Preclinical studies highlight their complementary actions in enhancing recovery and reducing scarring

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Observation: Gel did not form, when phase2 was added to phasel it got precepted out

This case highlights the importance of precautionary G6PD deficiency testing in patients that are at high risk for TLS and may receive rasburicase