MERTK and neoplasm: With regard to Mer, a recent study demonstrates that Mer RTK is overexpressed in about 70% of NSCLC relative to surrounding normal lung tissue where Mer functions to enhance the proliferation of cancer cells and inhibits their apoptosis, thereby promoting chemoresistance [5]; moreover, knockdown of Mer expression by short hairpin RNA (shRNA) abrogated oncogenic phenotypes of tumor cells, including decreased clonogenic growth, improved chemosensitivity, and delayed tumor progression in animal models [5], thus identifying it as a potential therapeutic target in NSCLC [14].