In gastric cancer models, FGFR inhibition has been shown to activate the TAK1/AMPK axis and enhance autophagic flux, thereby enabling resistant cells to withstand metabolic and pharmacologic stress; concurrently, transcription factor EB (TFEB), a lysosome–autophagy master regulator, undergoes nuclear translocation to upregulate lysosomal and autophagy-associated gene programs, further strengthening cellular stress tolerance [289,290]. This evidence concerns the gene TFEB and gastric cancer.