Two of 11 (18.2%) had thalassemia major and 2/11 (18.2%) were affected by rare inborn errors of immunity (prolidase deficiency and STAT3 gain-of-function) not associated with a defect in DNA repair and hence not prone to develop toxic complications of HSCT.16–18 Three of 11 (27.3%) were previously treated with IO, while for 1 patient (9.1%) it was the second HSCT. This evidence concerns the gene STAT3 and prolidase deficiency.