Paradoxically, in TNBC models, ULK1 overexpression drives metastatic progression via two distinct mechanisms, including autophagy-dependent upregulation of EMT transcription factors (e.g., Snail) and extracellular matrix components (e.g., fibronectin), and hypoxia-mediated remodeling of the tumor microenvironment [47,48]. Here, ULK1 is linked to neoplasm.