Obvious mechanisms include altered receptor tyrosine kinase signaling conform with the coreceptor concept of HSPGs, as demonstrated for the MAPK pathway in HS2ST1 and HS3ST2 overexpressing cells (Vijaya Kumar et al., 2014, 2020), and altered signaling via the Wnt pathway, as exemplified by altered expression of the Wnt-dependent transcription factor TCF4 for both sulfotransferases, and by the Sdc-1 and Wnt-dependent modulation of a colon cancer stem cell phenotype (Katakam et al., 2020b). This evidence concerns the gene SDC1 and colonic neoplasm.