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This comprehensive analysis of SFNs multiscale mechanisms provides the necessary foundation for developing targeted therapeutic strategies that maximize its anticancer efficacy while minimizing potential resistance mechanisms

In TRPML1-deficient mice, an increase in p62 and a clearance defect in LC3-II were found, which shows that the complete autophagy flux was destroyed (Curcio-Morelli et al., 2010)

All primers are listed in Supplementary Table 1

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