Specifically, the presence of SSTR1 and the truncated splicing variant sst5TMD4 could exert relevant pathophysiological roles by regulating different tumor parameters in PCa cells [e.g., cell proliferation, migration and PSA secretion; disruption of the normal response to somatostatin analogs (SSAs)] [18,19,20]. This evidence concerns the gene SSTR1 and posterior cortical atrophy.