The observation that GSE1 is upregulated, while TACSTD2 is downregulated, in PCa, with an increased GSE1/TACSTD2 expression ratio defining patients with PCa (Figure 1), is not logically decoupled from the current dysregulated oncogene–tumor suppressor homeostasis paradigm associated with tumor initiation and progression. This evidence concerns the gene TACSTD2 and posterior cortical atrophy.