MCL1 is often overexpressed in malignant cells, particularly in leukemia where the NOXA/MCL1 ratio determines sensitivity to chemotherapy and BH3-memitic drugs.22 NOXA expression can be increased transcriptionally through p53-dependent and -independent mechanisms and also by regulating protein turnover.6 NOXA has a very short half-life (~30 min) and is degraded by the proteasome; however, its turnover is not entirely dependent upon ubiquitination.8 The rate of NOXA protein turnover could be affected by hyperthermia and influenced by the presence of HSP70. This evidence concerns the gene MCL1 and leukemia.