ZNF432 is a zinc finger protein that functions as a poly(ADP-ribose) (PAR) reader regulating DNA damage response and homologous recombination. Upon recruitment to DNA lesions through DNA- and PAR-dependent mechanisms, ZNF432 stimulates PARP1 activity and binds preferentially to single-stranded DNA, inhibiting EXO1-mediated resection 1. This dual function finely balances PARP inhibitor sensitivity and resistance; ZNF432 loss confers PARP inhibitor resistance while overexpression increases sensitivity 1. Beyond DNA repair, ZNF432 suppresses endometrial cancer progression by interacting with UPF1 and enhancing its ubiquitination, promoting degradation of pro-survival factors and inducing apoptosis 2. ZNF432 overexpression significantly inhibited endometrial cancer cell proliferation and tumor growth in xenograft models 2. Additionally, ZNF432 gene variants modulate bronchodilator response in asthma, with inhaled corticosteroids modulating the association between ZNF432 polymorphisms and treatment response 3. These findings establish ZNF432 as a multifunctional regulator of genome integrity with therapeutic potential in cancer treatment.