Given the diversity of the initial NeoAg-specific CD4+ T cell repertoire as soon as the response is able to be detected, it’s unclear if the changes to the relative ratios of phenotypic subsets throughout tumor growth are a result of changing conditions for initial priming of newly activated clones or a result of the environments, APC types available, and accessory signals inducing either preferential division in a limited subset of phenotypes or plasticity in the ongoing response. The gene discussed is CD4; the disease is neoplasm.