Cu-THBQ/AX impairs ATP7A function, triggers copper ion accumulation, instigates tumor cell cuproptosis, and activates the in situ type I photodynamic action of Cu-THBQ/AX via alkaline phosphatase overexpressed on the tumor cell membrane, generating O2− and ·OH, inducing caspase-3-mediated pro-inflammatory pyroptosis, thereby effectively transitioning the tumor microenvironment from a “cold” state to a “hot” state, suppressing tumor growth and metastasis. The gene discussed is CASP3; the disease is neoplasm.