Moreover, considering the extracellular localization of TGFBI as a matrix component, its deregulation (already visible at 48 h post-EBV infection and dependent on LMP1 viral oncoprotein expression, which is progressively lost in advanced stages of eBL) might be an early driver of transformation, contributing to a permissive tumor microenvironment for cancer initiation. This evidence concerns the gene PDLIM7 and Epstein-Barr virus infection.