Breast cancer is an established immunologically cold tumor, which is a phenotype that recent evidence suggests is augmented by tumor cell driven hematopoiesis. In their study, Wang and colleagues evaluated the impact of kindlin-2, a highly expressed adapter protein that the authors have previously linked to macrophage polarization and tumor infiltration, on the immune response in triple-negative breast cancer (TNBC) using multiple in vivo models. TNBC mouse models bearing kindlin-2 expressing tumors revealed increased levels of myeloid cells in the blood and bone marrow compared to their naive counterparts, indicating that TNBC influences hematopoietic reprogramming through increased myelopoiesis. Alternatively, kindlin-2 knockout tumor-bearing mice showed increased infiltration of cytotoxic T cells, activation of immune checkpoint molecules, and loss of PD-L1 expression, suggesting an immune evasive role for kindlin-2. The cover image illustrates this heightened immune infiltration in kindlin-2 knockout tumors. The authors further confirmed the role of kindlin-2 in anti-tumor immune evasion using anti–PD-L1 therapy in vivo, observing comparative kindlin-2–mediated tumor progression upon PD-L1 inhibition. This article can be found on page 450.