Excess SCD5 expression evokes a chronically greater ratio MUFA-to-SFA in cells, with consequent alterations in key metabolic and signaling pathways involved in cell proliferation, differentiation and survival. While the molecular mechanisms by which SCD5 is linked to developmental and neurological pathologies, as well as in and cancer, remain to be elucidated, human genetic data and experimental studies suggest that abnormal SCD5 may be implicated in the onset and progression of disease.