In vivo tumor growth of inoculated B16/F10 was delayed by TIGIT deficiency, while exhaustion of effector cells (CTL and NK cells) targeting tumor was reversed by in vivo TIGIT blocking in combination with in vivo Flt3L overexpression by gene delivery and improved overall survival by significantly suppressing pre-established B16/F10 tumor growth and metastasis (151). Here, FLT3LG is linked to neoplasm.