Specifically, In1-ghrelin increased malignant-features of PCa cells by altering the expression of key-oncogenes, tumor-suppressor genes and genes associated to PCa pathophysiology such as APC, CAV1, SFRP1, NRIP1, CDKN2A, IGFBP5 and LOXL1 [36–41], which could help to explain the functional changes triggered by In1-ghrelin over-exposition (treatment and/or overexpression). Here, GHRL is linked to posterior cortical atrophy.