Inflammation is the common denominator to the postnatal events that overlap with lymphatic vessel growth, or lymphangiogenesis. Undoubtedly, inflammation and accompanying fluid overload are cardinal factors in wound healing, lymphedema, the pathogenesis of some forms of lymphangiomatosis, and solid tumor lymphangiogenesis. The assertion that inflammation actually triggers lymphangiogenesis lies in the evidence set forth below that inflammation is the usual precursor to tissue repair and regeneration. Moreover, the panel of pro-inflammatory and anti-inflammatory molecules that orchestrates the inflammatory response abounds with cytokines and chemokines that foster survival, migration, and proliferation of lymphatic endothelial cells. Finally, both interstitial fluid overload and increased demand for removal of leukocytes can benefit from lymphangiogenesis, although the mechanisms controlling the exit of leukocytes from tissues via the lymphatics are practically unknown. The pertinent question actually is how and why inflammation presents with formation of new lymph vessels in liver fibrosis but not in rheumatoid arthritis. One possible explanation is that organspecific histological and functional properties of the lymphatic endothelium gauge their response to death, survival, and proliferative factors. Alternatively, the decision to remain quiescent, proliferate or regress resides within the stroma microenvironment.