In tumors with high endogenous HMGCR expression and abundant TNF-α (e.g., HER2+/TNBC breast cancer), statin-mediated HMGCR-TNF-α interactions are more pronounced, manifesting as: reduced HMGCR expression, suppressed TNF-α production, and consequently weakened pro-inflammatory/pro-angiogenic signaling. The gene discussed is HMGCR; the disease is breast cancer.