Previous studies show that Batf3-dependent CD8a+ and/or CD103+ cDCs play an essential role in antitumor immunity which can exploit Axl activation as an intrinsic negative feedback to inhibit ongoing immune response [17, 25–28], we therefore assessed the impact of Axl inhibition on the prevalence and activation status of cDCs at the tumor site, focusing on the CD103+ subset. Here, AXL is linked to neoplasm.