The cGAS-STING pathway in NAFLD/ALD reveals that it functions as a common inflammatory amplifier, yet is engaged by disease-specific triggers and elicits distinct pathological consequences—exemplified by the dual-edged role of STING deficiency, which is protective against acute inflammation but potentially detrimental to chronic metabolic adaptation. This evidence concerns the gene STING1 and metabolic dysfunction-associated steatotic liver disease.