Targeting MCs within the TME presents an immunotherapy opportunity to remodulate the TME from an immunosuppressive “cold” state into a “hot” state, marked by reduced immunosuppression, depletion of pro‐tumor cells such as TAMs, and increased infiltration of anti‐tumor effector cells like CD8+ T‐cells.[34] To demonstrate that MCTN can target the TME, we examined the biodistribution of MCTN‐luciferase in subcutaneous MC38 tumor‐burdened C57BL6 mice (Figure S10, Supporting Information). Here, CD8A is linked to neoplasm.