The first hints that DYRK2 may influence carcinogenesis were derived from a genomic analysis and differential gene expression studies, highlighting DYRK2 overexpression in association with the amplification of its genomic locus in esophageal and lung adenocarcinomas [128,129], GIST [130], gastric adenocarcinoma [131] and liposarcoma [132]. Here, DYRK2 is linked to gastrointestinal stromal tumor.