Moreover, lesions affecting these genes cooperate with IL7R mutation, likely contributing to increased proliferation, as shown by our studies with mutant Kras and consequent upregulation of Ccnd2, and those of Geron et al., which showed deletion of CDKN2A in a B-ALL arising from the in vivo transplantation of human cord blood progenitors transduced with mutant IL7R and demonstrated cooperation between IL7R mutation and CDKN2A deletion in driving human B-ALL (10.1101/2020.01.27.919951). The gene discussed is KRAS; the disease is precursor B-cell acute lymphoblastic leukemia.