I hypothesize that feline chronic gingivostomatitis (FCGS) arises from an interplay between genetic predisposition and dysregulated immune responses to environmental or viral triggers, which drive chronic inflammation in the oral mucosa. This project will focus on studying 1) genetic factors and 2) molecular drivers underlying disease development.

 Thus, my two-sub hypothesis are as follows:
1. I hypothesize that genetic risk factors confer susceptibility to FCGS and impair immune system function in affected cats. This will be tested through a genome-wide association study (GWAS).

2. I hypothesize that FCGS-affected tissues are enriched for immune cell populations with altered gene expression and chromatin accessibility patterns. This will be tested using single-nucleus RNA sequencing (snRNA-seq) and single-nucleus Assay for Transposase-Accessible Chromatin (snATACseq).