For example, recent in vitro observations indicated that silencing of PART1 substantially sensitized the response of TE1 and KYSE-450 esophageal squamous cell carcinoma (ESCC) cells to gefitinib, while upregulation of PART1 led to sequestering of miR-129 and the resultant upregulation of Bcl-2, thereby conferring ESCC cells resistance to gefitinib [45]. This evidence concerns the gene PART1 and esophageal squamous cell carcinoma.