NR0B2 and neoplasm: Of relevance in the context of CRCs, both SHP1 (14) and SHP2 (15) have been found to serve as brakes that limit tumorigenesis via their ability to antagonistically inactivate pro-oncogenic tyrosine-based signals; mice lacking SHP1/2 in intestinal epithelial cells (IECs) develop higher tumor burden, associated with sustained activation of downstream pathways such as the PI3K/Akt, Wnt/β-catenin, NF-κB, and STAT3 signals.