MKI67 and neoplasm: Indeed, numerous clinical studies have suggested MYC overexpression as a marker for poor outcomes in TNBC patients through various pathways and mechanisms, including: (i) promoting cell proliferation and survival via PI3K, (ii) mediating mammary stem cell amplification as a cascade of Wnt/β-catenin activation, (iii) accelerating cell cycle activity associated with a high expression of cyclin B1 and Ki67, and (iv) enhancing tumor angiogenesis by activating VEGF signaling [87,88].