In NB, the induction of CD44V isoform (especially CD44v6) expression by 12-O-tetradecanoyl phorbol-13-acetate (TPA), IGF-1, and PDGF was correlated with an increased cellular binding to hyaluronic acid (a major counterreceptor for CD44; free form of GAGs in ECM) by phosphoinositide 3-kinase (PI3K)/protein kinase C (PKC) pathways, indicating the impact of glycosylation status and local distributions of the molecule on the changes in NB cell properties (Fig. 3) [98]. This evidence concerns the gene CD44 and neuroblastoma.