To evaluate the role of FN-EDA in the development of ocular hypertension, we utilized an adenovirus vector to overexpress bioactivated TGFβ2 in the TM of mice containing a constitutively active FN-EDA isoform or in FN-EDA null mice, with or without mutation in Tlr4. Here we found that TGFβ2-induced ocular hypertension and ECM production is dependent on both EDA and Tlr4, and in mice constitutively expressing FN-EDA the effects of TGFβ2 are amplified (Roberts et al., 2020). This evidence concerns the gene TGFB2 and ocular hypertension.