Pharmacologic EGFR inhibition in nonresistant CRCs is associated with compensatory FGFR2-induced p38/MAPK upregulation [72, 89] that induces the downstream proinflammatory mesenchymal mitogen IL-1α [90–94] which in turn promotes both sporadic acne [95] and iatrogenic folliculitis [96, 97]. The gene discussed is IL1A; the disease is acne.