PIM3 and acute myeloid leukemia: However, these unaffected proteins were reported to be involved in the apoptosis of MV4-11 cells in other studies e.g., loss of ataxia telangiectasia mutated (ATM) mitigated the effect of miR-100 exhaustion on cell viability and apoptosis in AML cells [31], provirus integrating site moloney murine leukemia virus 3 (PIM3) overexpression enhanced AML cell proliferation and inhibited instinctive apoptosis by phosphorylating BAD (pBAD) at Ser112 [32], and Polyphyllin I affected the apoptosis of AML cell lines by regulating expression of phosphorylated-JNK [33].