ZNF862 is a zinc finger protein localized to the cytoplasm that functions as a transcriptional regulator controlling gingival fibroblast proliferation and apoptosis 1. ZNF862 overexpression inhibits fibroblast proliferation by suppressing the p21-RB1 cell cycle checkpoint pathway, inducing G0/G1 phase arrest, while simultaneously promoting apoptosis through activation of the Bcl-xL-Caspase 3 pathway 1. At the molecular level, ZNF862 mutations associated with hereditary gingival fibromatosis (HGF) increase profibrotic collagen synthesis, particularly COL1A1, leading to excessive gingival tissue overgrowth 2. ZNF862 represents one of three identified genes (alongside SOS1 and REST) causing autosomal-dominant HGF, a rare genetic condition affecting approximately 1:750,000 individuals 3. Beyond gingival disease, ZNF862 shows epigenetic associations with IgE-mediated type-I hypersensitivity in early childhood development 4 and appears in prognostic models for prostate cancer progression 5. The gene has also been identified as carrying recurrent mutations in breast cancer precursor lesions 6. These findings establish ZNF862 as a multifunctional regulator with primary significance in controlling cellular differentiation and fibroblast homeostasis.