Cyclin-dependent kinases 4 and 6 (CDK4/6) are important mediators of cellular proliferation. Inhibitors of CDK4/6 have shown promising clinical activity in breast cancer. While the key mechanism of their anti-tumor activity relies on inhibition of cancer cell proliferation, accumulating evidence suggest that CDK4/6 inhibitors can also affect tumor-immune interplay. However, the mechanism of how CDK4/6i modulates anti-tumor immunity is not fully characterized. Here we show that treatment with CDK4/6i promotes recruitment of endogenous and adoptively transferred T cells into the tumor in two immunocompetent murine mammary models with distinct genetic backgrounds. T cells were recruited by chemokines CCL5 and CXCL9, 10, and 11 that were secreted by CDK4/6i-treated tumor cells. Mechanistically, chemokine secretion was driven by oxidative stress induced by prolonged exposure to CDK4/6i. We demonstrated that CDK4/6i-treated cells maintain active PI3K/mTOR pathway which is a master regulator of cell metabolism. Without metabolic demands of proliferation in CDK4/6i-arrested cells, metabolic fluxes led to accumulation of ROS and subsequent induction of inflammatory stress response. Accordingly, removal of ROS, inhibition of glucose and glutamine uptake and their catabolism, as well as, inactivation of PI3K or mTOR abrogated chemokine secretion in CDK4/6i-treated cells. We also show that chemokine-mediated T cell recruitment associated with CDK4/6i therapy augments anti-tumor activity of immunotherapies in a murine preclinical model including T cell co-stimulatory therapy with agonistic OX40/4-1BB antibodies and adoptive T cell transfer therapy. In summary, our findings demonstrate that CDK4/6i can promote T cell recruitment into the tumor by inducing chemokine secretion in tumor cells. This raises a possibility of utilizing CDK4/6i to stimulate anti-tumor immunity and immunotherapy response in immunologically silent tumors.