In addition to hypoxia, which is a major driver of CAIX expression by cancer cells [6,9], CAIX can also be induced in normoxia by high cell-density-mediated pseudohypoxia [10,11], and by hypoxia-independent mechanisms such as lactate- [12] and redox-mediated [13] stabilization of HIF-1α. Here, HIF1A is linked to cancer.