SOAT1 and neoplasm: The growth of GlcT mutant clones appeared to cause a general increase of EGFR and JAK/STAT activities within the intestinal epithelium, as many differentiated cells also exhibited EGFR or JAK/STAT signaling activation (Figure 4—figure supplement 1), which is likely due to stress responses induced by tumor growth (Patel et al., 2015).