As such, precisely ascribing various phenotypic alterations in esophageal cancer cells to effects of A279T on canonical versus non-canonical telomerase activities may be quite difficult, particularly in light of recent observations that TERT over-expression increases growth of primary epithelial cells via processes, which are independent of TERT catalytic activity, chromosomal capping, or Wnt β-catenin signaling [55]. This evidence concerns the gene TERT and esophageal cancer.