Liver allografts in pigs and rats can induce tolerance; both hepatocytes and passenger bone-marrow-derived cells are necessary. 1, 2 Grafted livers recover spontaneously from histological and biochemical acute rejection. A short course of high-dose cyclosporin in renal allografted pigs given with donor splenocytes or donor blood resulted in “operational tolerance” with good graft function for more than 1 year in half the animals. 3 These and other observations support the hypothesis that, in the absence of an aggressive T-cell response, an engagement of the immune system can lead to tolerance. Knechtle and colleagues found that T-cell depletion induced by a CD3-diphtheria immunotoxin given before renal allografting produced tolerance to renal allografts in rhesus monkeys. Prolonged donor-skin-graft survival in most of these animals was convincing evidence of a tolerant state. 4 Campath 1H, a humanised anti-CD53 antihypertensive actions of NO combined with the ability of heparin to inhibit smooth muscle hypertrophy and stimulate new vessel growth may provide a theoretical basis for prolonged treatment of primary pulmonary hypertension. This might be particularly applicable to infants who have substantial capacity for smooth muscle regression, alveolar growth, and angiogenesis. Moreover, the potential to induce accelerated maturation of the pulmonary vasculature in patients with congenital heart disease may make plausible certain surgical interventions previously thought impossible in the newborn baby.