To bridge the gap between mildly acidic TME and pH required for ideal Fenton reaction (pH 3–4), Bu and coworkers fabricated carbonic anhydrase IX inhibitor (CAI) on the surface of AFeNPs (AFeNPs@CAI) to reconfigure tumor acidosis (Figure 1B).[35] The inhibition of overexpressed carbonic anhydrase IX in cancer cells resulted in extracellular alkalinity increase and intracellular acidity decrease, which in turn was beneficial for augmenting the efficiency of Fenton reaction and hence •OH‐mediated oxidative damage of tumor through self‐enhanced CDT. Here, CA1 is linked to neoplasm.