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Molecular analyses showed that CO23RFLC had acquired a marked increased expression of the MDR1 gene encoding for an efflux pump protein mainly responsible for the drug-resistance, due to a mutation in the transcription factor gene MRR1 [16] whereas CO23RFK had a homozygous mutation (S645Y substitution) in the FSK1 gene, responsible for the synthesis of glucan [17]

UC patients show increased ILC1s and ILC2s frequencies but decreased NKp44 + ILC3s, which are crucial for IL-22-mediated epithelial barrier protection [80]

It can effectively delay premature cell death, and increase cell regeneration

Mitochondrial dysfunction, impaired axonal transport, and neuroinflammation are key contributors to oxidative stress in ALS [169]