Based on our findings, we proposed that sequential therapy may be a more optimal dosing strategy, whereby early treatment with a CDK4/6 inhibitor promotes the formation of a more durable memory T cell pool that can later serve as a substrate for PD-1 blockade, and we validate this hypothesis in a mouse model of melanoma of neoadjuvant treatment of melanoma and breast cancer. The gene discussed is PDCD1; the disease is melanoma.