As to the source of IGF1, a recent study has revealed how, in the thymic microenvironment of murine T-ALL models and T-ALL primary patient samples, leukemic cells overexpressed IGF1R while tumor-associated dendritic cells (DCs) synthesized and released IGF1, which drove T-ALL growth ex-vivo [85]. This evidence concerns the gene IGF1 and acute lymphoblastic leukemia.