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The oversimplified interpretation of SERM action described by agonist/antagonist was no longer acceptable for nuclear hormone physiology

Supplementation may help lower this risk

G3BP1 is required for TFE3 nuclear translocation to suppress lipogenesis A recent study reported that hepatocyte-specific genetic deletion of FLCN in adult mice provided protection against both MASLD and MASH, and showed that these protective effects are dependent on the nuclear translocation of Transcription factor E3 (TFE3), a master transcriptional regulator with widespread impacts on processes including (but not limited to) lysosome biogenesis and lipolysis 37,38,39,40

Several studies using HCC cell lines suggests that ferroptosis may serve as the principal mechanism underlying the anticancer effect of sorafenib via suppressing the cystine/glutamate antiporter SLC7A11 [94,95,96]