At least part of the mechanism by which GFI1 supports the survival of T-ALL is by prevention of p53-induced apoptosis via GFI1 interaction with the p53 C-terminus leading to the recruitment of LSD1 to demethylate p53, which decreases the acetylation of p53—thus blocking p53 from activating pro-apoptotic target genes [10,11]. The gene discussed is GFI1; the disease is acute lymphoblastic leukemia.