However, it needs to be noted that the suppression of KMT2C alone does not suffice to induce leukemogenesis, and the cellular background also plays a role, including p53 loss (p53−/− HSCPs), which cooperates with KMT2C to impair the differentiation of these cells, leading to a myelodysplastic syndrome (MDS)-like state. The gene discussed is TP53; the disease is myelodysplastic syndrome.