H2AZ1 and breast cancer: In addition to the fact that histone H1 poly-ADP-ribosylation causes histone H1 eviction from promoters of cfos in depolarized cerebral neurons,51,52 in MCF-7 human breast cancer cells, histone H1 poly-ADP-ribosylation is mediated by poly-ADP-ribosylation of the demethylase KDM5B, which maintains methylation on histone H3 (H3K4me3) adjacent to promoters of transcribed genes.8 In another mechanism, in HeLa cervical cancer cells, PARP1 activation causes local destabilization of chromatin at cfos promoters by facilitating the exchange of the variant histone H2A.Z with histone H2A.64,65