In the same year, they reported another folate-cagedPROTAC 11 (Table 1, entry 11) designed by attaching a folate group to the pomalidomidemoiety of reported ALK PROTAC via a glutathione (GSH)-sensitive linker.62 Similar to PROTAC 10, PROTAC 11 showed FOLR1-dependent NPM-ALK fusion protein degradation.This strategy provides an approach for the targeted delivery of folate-cagedPROTACs to FOLR1-expressing cancer cells with the potential to amelioratetoxicity.62 This evidence concerns the gene ALK and cancer.