To assess the relevance of NOXA/MCL1 turnover for tumour cell survival, we generated NOXA-KO derivatives from these three TNBC cell lines using two independent sgRNAs targeting NOXA. While the steady-state levels of MCL1 did not substantially differ in asynchronous cells, we could observe a clear stabilisation of MCL1 in the absence of NOXA compared to parental cells upon extended M-arrest (Fig. 5). The gene discussed is MCL1; the disease is neoplasm.