Clinically, risk stratification must extend beyond traditional cardiovascular history to incorporate cardiometabolic and functional phenotyping—including visceral adiposity, insulin resistance, metabolic syndrome, NAFLD, sarcopenia, micronutrient deficits, and inflammatory burden—because these factors amplify susceptibility to anthracyclines, HER2 agents, TKIs, proteasome inhibitors, and immune-checkpoint inhibitors and modulate both the timing and the sensitivity of surveillance [63]. This evidence concerns the gene ERBB2 and metabolic dysfunction-associated steatotic liver disease.