Fig. 7
![Fig. 7](http://media.springernature.com/full/springer-static/image/art%3A10.1186%2Fs12964-023-01259-1/MediaObjects/12964_2023_1259_Fig7_HTML.png)
Mechanistic model of the role of miR-24-3p: miR-24-3p regulates T-cell apoptosis induction. Signal I: When TNF binds to TNFR1, it leads to the activation of cell survival via the activation of the NF-κB signaling network and JAK/STAT proteins and hence apoptotic resistance. Signal II: Overexpression of miR-24-3p through derived EXOs silences DENN/MADD expression, which induces the apoptosis signaling network through the deregulation of NF-κB and JAK/STAT and ERK phosphorylation. miR-24-3p increases the expression of caspase 9 and 3, inducing apoptosis. Finally, miR-24-3p impedes T-cell function through the Jak/STAT and NF-κB signaling networks. miR-24-3p is therefore a key player in AML escape from T-cell-mediated cytotoxicity and largely contributes to blast survival