When these kinases are inactivated by their displacement from Sdc4 by SSTNEGFR, a corresponding increase in p38 mitogen-activated protein kinase (p38MAPK) occurs, presumably constitutively activated by metabolic, oncogenic, and/or genotoxic stress in the tumor cells but held in abeyance by signaling from the Sdc4 receptor complex. The gene discussed is SDC4; the disease is neoplasm.