We observed overexpression of ARL6IP1, the substrate of HuD, significantly protects cells against HuD silencing (Fig. 7B and S6B) in NB cell lines (IMR-32, SK-N-SH and SK-N-DZ); moreover, silencing of ARL6IP1, by itself, reduces cell viability (Fig. 7C and S6C) and its forced overexpression partially compensates for HuD knockdown (Fig. S6D). This evidence concerns the gene ELAVL4 and neuroblastoma.