Contrary to that data, a recent study found RNAi–mediated knockdown of SCYL1 in MDA-MB-231 cells did not alter REST steady-state level and turnover; thus, SCYL1 is dispensable for the down-regulation of REST [26], suggesting in some cases the function of SCYL1 in tumor progression may not be dependent on degradation of REST. This evidence concerns the gene SCYL1 and neoplasm.