Shown are potential mechanisms of cell growth regulation in ARMS versus ERMS tumor cells related to signaling through ILK, JNK1, and c-Jun. ILK functions are regulated through signals initiated by ECM-integrin interactions or growth factor (GF) stimulation (6). In more clinically favorable cases of ERMS, Durbin et al. (10) demonstrate, in their study in this issue of the JCI, that ILK suppresses phosphorylation of JNK1 and c-Jun, thereby preventing accelerated cell proliferation. While the exact mechanism remains to be shown, the repression of JNK phosphorylation by ILK in this tumor subtype may occur through additional intermediates, including a complex of ILK-associated serine/threonine phosphatase 2C (ILKAP) with apoptosis signal–regulating kinase 1 (ASK1). In ARMS, JNK1 levels are diminished by the PAX3-FKHR oncoprotein, thereby leaving other pathways open to modulating or inducing c-Jun phosphorylation and accelerating cell proliferation. In these tumors, the oncogenic effects of ILK may involve regulation of JNK1 phosphorylation, as suggested by Durbin et al., and/or ILK-induced activation of α-NAC. RTK, receptor tyrosine kinase.