Thus, when viewed together, our results indicate that In1-ghrelin splicing variant is overexpressed in PCa, where it can regulate cell proliferation, migration, tumor growth and PSA secretion, through the modulation of the activation of certain signaling-pathways (ERK phosphorylation) and the expression of several oncogenes and tumor-suppressor genes, thereby suggesting a possible pathophysiological role for this splice-variant in human PCa. Here, GHRL is linked to posterior cortical atrophy.