Strategies to enhance the stemness and persistence of antitumor T cells are being actively pursued given the central role of stem-like cells in eliciting productive antitumor responses.3,8 Several pathways and relevant players influencing the formation of these cells have been characterized in preclinical tumor models offering exploitable targets for potentiating T-cell therapy.9–14 By using CRISPRa gain-of-function screens, we aimed to broaden actionable targets to augment CD8+ T-cell stemness beyond normal physiology. Here, CD8A is linked to neoplasm.