Additionally, considering the association between TP53 mutations and Venetoclax resistance [30], and given that ATF4 mediates the transactivation of the MCL-1 antagonist NOXA [31], we checked the impact of DELE1 expression (+/- TP53 mutations) on Venetoclax response using both Leucegene and BEAT AML data [32], but again did not identify any collaborative effect (Figs. S9 and S10). This evidence concerns the gene ATF4 and acute myeloid leukemia.