Recently published studies have shown that pharmacologic inhibition of CAIX activity in vivo in a model of glioblastoma multiforme (GBM)—when used in combination with the standard of cancer chemotherapy, temozolomide—results in an altered flux of AAs, including essential AAs such as leucine [31], potentially linking CAIX to EAA transport through an association with LAT1, although the mechanism remains to be determined. This evidence concerns the gene CA9 and cancer.