For instance, the instability of the carboxylic ester‐based linker in XMT‐2056 led to the inevitable off‐target toxicity in clinic trials.[20] Similarly, the limited tumor penetration of CDN STING agonist IMSA172 resulted in the limited antitumor efficacy of αEGFR‐172 ADC[18] in vivo. This evidence concerns the gene NT5C and neoplasm.