Indeed, a similar scenario has been shown previously for a mutated type I interferon with a decreased receptor affinity.[58] The injection of the mutated cytokine conjugated to an Nb targeting Clec9A, expressed by XCR1+ cDC1s, in tumor‐bearing mice drastically decreased tumor growth, indicating that the activity of the mutated cytokine is selectively restored for cell populations expressing Clec9A, while minimizing systemic toxicity. Here, CLEC9A is linked to neoplasm.