A study from Rachel and colleagues found that CAR-T cells engineered to overexpress the canonical AP-1 factor c-Jun have enhanced expansion potential, increased functional capacity, diminished terminal differentiation, and improved antitumor potency in five different mouse tumor models and concluded that a functional deficiency in c-Jun mediates dysfunction in exhausted human T cells, and the overexpression of c-Jun renders CAR-T cells resistant to exhaustion.99 Here, JUN is linked to neoplasm.