When WNT/STOP is off, GSK3-dependent protein degradation remains unperturbed and produces catabolic free Asn which induces ASNase resistance in CRC; whereas CRCs with R-spondin (RSPO) fusions such as RSPO3 have activated WNT/STOP which inhibits the proteasome, limiting Asn availability and thus increasing vulnerability to ASNase (Hinze et al., 2020). This evidence concerns the gene RSPO1 and colorectal carcinoma.