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Coincidingly, the noncytotoxic reduction in RBL-2H3 degranulation by B-FAHF-2 (2 g/mL) was established [30]

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In contrast, MYC was more activated in HCC tumors showing no benefit of the treatment, suggesting that MYC may trigger resistance of HCC cells to sorafenib

However, these models fail to explain how disease-specific monomeric Syn variants orchestrate the sequestration of diverse cellular proteins and damaged membrane organelles to initiate and promote LB formation