Together, these observations suggest that there may be cooperation between the IGF1-IGF1R and KITLG–KIT signaling pathways both in normal tissues and certain cancers including GIST; these interactions may be mediated by epigenetic control of gene transcription; and increased Kitl/KITLG expression may result in autocrine/paracrine stimulation of proliferation in cells expressing WT KIT. The gene discussed is IGF1R; the disease is gastrointestinal stromal tumor.