IL-17 signaling links wound healing to tumor growth. (A) IL-17 stimulates the proliferation of Lrig1⁺ cells and promotes the expansion and migration of their progeny. Expanded Lrig1⁺ progeny migrate out of the hair follicle and participate in reepithelialization. In the presence of oncogenic mutations such as KrasG12D, the IL-17–expanded progeny of Lrig1⁺ cells contribute majorly to wound- or inflammation-induced tumor tissue. (B) IL-17 stimulation in Lrig1⁺ cells leads to the recruitment of EGFR by TRAF4 to the IL-17R complex. The IL-17R adaptor Act1 then recruits Src to the receptor complex, resulting in the transactivation of EGFR. EGFR subsequently phosphorylates MEKK3, initiating the MEKK3–MEK5–ERK5 cascade. RA, IL-17 receptor A; RC, IL-17 receptor C; SRC, proto-oncogene tyrosine-protein kinase Src; TK, tyrosine kinase domain. Reprinted with permission, Cleveland Clinic Center for Medical Art & Photography © 2019. All rights reserved.