Overall, the present work reveals that LG damage that simulates trauma, surgical intervention, radiotherapy, or long-term disease, as observed in SjD or GvHD that terminate with LG atrophy or fibrosis, is dominated by prolonged inflammatory mediators, such as TNF-α and MMP-9 and others, and extension of the inflammation to the LFU. The gene discussed is TNF; the disease is graft versus host disease.