However, melanomas evolve intrinsic mechanisms, such as increased signaling via β-catenin or secretion of prostaglandin E2 (PGE2), to selectively block recruitment of cDC1.9, 18 Our work suggests that, in addition to these tumor-intrinsic mechanisms, the tumor hematopoietic compartment also determines the composition of resident myeloid cells, and this can be re-set upon depletion of CD11c+ cells. Here, ITGAX is linked to melanoma.