Despite the lack of effective antibodies targeting DELE1 (as already reported by Guo et al. [11]), immunoblotting quantification of different factors of the pathway in OCI-AML1 (TP53-WT) and HL60 (TP53-null) AML cells upon 4 and 24 h CCCP exposure – a mitochondrial ionophore used as an alternative ISR-inducing drug by Fessler et al. for DELE1 characterization [10] – showed that a downregulation of DELE1 gene expression was sufficient to prevent OMA1–DELE1–HRI pathway induction in both cell lines in a TP53-independent manner (Fig. 3D, Fig. S5). This evidence concerns the gene TP53 and acute myeloid leukemia.