TINAG (tubulointerstitial nephritis antigen) is a non-catalytic peptidase C1 family protein located on chromosome 6 that mediates adhesion of proximal tubule epithelial cells through integrin interactions with alpha3-beta1 and alphaV-beta3 integrins. The protein localizes to basement membrane and lysosomal compartments and possesses cysteine-type endopeptidase activity. Beyond its established renal tubular function, TINAG has emerged as a multifactorial disease susceptibility gene. Genome-wide association studies identified TINAG as a significant locus for dermatophytosis susceptibility, with the rs16885197 missense variant conferring a 7.8-fold increased odds ratio for infection 1. In hepatocellular carcinoma, TINAG overexpression promotes proliferation, invasion, and migration through PI3K/AKT pathway activation, independent of its adhesion function, suggesting oncogenic roles in epithelial malignancies 2. A heterozygous stop-gain mutation (c.G2A, p.W2*) in TINAG was identified as a loss-of-function genetic cause of pectus excavatum, indicating that TINAG regulates osteoblast proliferation 3. Additionally, TINAG was identified within a nine-gene basement membrane-related signature predictive of colorectal cancer prognosis 4, and associated with glaucoma medication non-adherence 5. These findings establish TINAG as a pleiotropic gene with roles in cell-matrix interactions, infection susceptibility, and cancer progression.