In contrast, NCLs caused by mutations in lysosomal enzymes such as TPP1 (causing CLN2 disease) are amenable to ERT, due to the ability of the protein to cross-correct (traffic to the extracellular space and then be taken up by other cells), and interim results from the CLN2 disease ERT trial, in which recombinant protein is delivered to the CSF, look promising (Clincaltrials.gov identifier NCT01907087; http://investors.bmrn.com/releasedetail.cfm?ReleaseID=958565; [20]. Here, TPP1 is linked to glycogen storage disease VI.