Cytoplasmic Linker Protein-115 (CLIP-115) is encoded by the gene CYLN2, which is hemizygously deleted in patients with Williams-Beuren Syndrome (WBS). Phenotype-genotype correlation with patient data and the behaviour of Cyln2 knockout mice suggest that CLIP-115 has an essential role in normal neuronal functions. Therefore, its role in neurite formation was examined by interfering with its normal protein function via overexpression of several CLIP-115 fragments in a neuronal cell line, and analyzing parameters that were related to neurite formation (total neurite length and number, and neurite branching). Overexpression of CLIP-115 full length protein seemed to increase both neurite length and number, whereas overexpressing CLASP interacting domain of CLIP-115 might have negative effect on neurite length. Cells expressing full length CLIP-115 had a significantly higher frequency of being multinucleated, suggesting that similar to its homologue CLIP-170, and its interacting partner CLASP, CLIP-115 also functions in the process of cell division and cytokinesis.