The tryptophan–indole branch in breast cancer appears to act primarily through tumor-intrinsic metabolic restraint rather than direct T-cell programming: expansion of Prevotella copri depletes host IPyA, relieving UHRF1-mediated repression of AMPK and thereby promoting tumor growth; restoring IPyA re-engages AMPK signaling and slows progression [107, 114]. This evidence concerns the gene UHRF1 and breast cancer.