PPP4R3B is a regulatory subunit of protein phosphatase 4 (PP4), a critical regulator of DNA damage response (DDR) and immune signaling. As a component of the PP4 complex, PPP4R3B likely modulates serine/threonine phosphatase activity at centrosomal and nuclear sites, influencing double-strand break repair and chr2 dynamics 1. Functionally, PPP4R3B participates in coordinating cellular responses to DNA damage and genotoxic stress. PP4 inhibition or PPP4R3B knockdown combined with chemotherapy triggers robust inflammatory signaling through NF-κB and STAT1 activation, increasing pro-inflammatory cytokine expression (CCL5, CXCL10, IL-6) and type I interferon responses 1. These events enhance recruitment and activation of immune effector cells, including NK cells and CD8+ T cells, promoting anti-tumor immunity 1. Clinically, PPP4R3B dysfunction has been associated with psoriasis susceptibility, identified through exome-wide rare loss-of-function variant analysis in Han Chinese populations 2. The gene's role in both cancer immunotherapy and inflammatory disease suggests PPP4R3B functions as a nodal regulator integrating DNA damage signals with immune activation pathways. These findings support investigating PP4/PPP4R3B inhibition as a potential therapeutic strategy to enhance chemo-immunotherapy responses in ovarian cancer and other malignancies.