SREBF1 and metabolic dysfunction-associated steatotic liver disease: Therefore, we revealed a previously unappreciated role for dysregulated mTORC1 signaling in promoting cancer-initiating events via activation of STAT5, wherein mTORC1 upregulates SREBP1 transcription via crosstalk with the STAT5 pathway, which contributes to the NAFLD-related HCC pathogenesis.