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However, the mechanism of the progress is still unclear

[ 14 ] BACH1 can also recruit a histone H3K4me1/2 demethylase named lysinespecific demethylase 2 (LSD2), bind to p53 R175H and form BACH1p53 R175H LSD2 complex, which modifies histone methylation status at the promoter of BACH1 targets and subsequently activates the genes transcription

Despite the fact that response rates were comparable between the two arms, this immune/targeted triplet was observed to significantly lengthen the duration of response (DoR) and progression-free survival (PFS) [221]