As a consequence, EVI1 interferes with the interaction of JNK with its substrates, effectively resulting in a block of UV/ TNF-α-induced JNK kinase activity and cell death.67 More recently, it has also been shown that EVI1 can modulate p53 at the protein level, by influencing its stability and thus protein abundance68 (Figure 2C), which has been linked with resistance of EVI1high AML cells to chemotherapy. Here, MECOM is linked to acute myeloid leukemia.