Chen et al. (2020) recently demonstrated that the PCa microenvironment triggered the expression of Activin A via NF-kappaB stimulation. These high levels of Activin A also enhanced the development of an aggressive ALDHhi phenotype through a Smad and ERK1/2 driven pathway. Finally, a very recent study by Hou et al. tried to investigate the regulation of prostate CSCs by thrombospondins 4 (THBS4). It was revealed that HBS4 silencing can hamper the development of PCa characteristics via blockade of the PI3K/Akt pathway (Hou et al., 2020). The gene discussed is AKT1; the disease is posterior cortical atrophy.