Here, we tested these hypotheses by investigating the effects of IGF1 on endogenous Kitl/KITLG expression and the underlying epigenetic mechanisms and signaling pathways in IGF1R-expressing cells and tissues including gastric smooth muscles [18-20,22], the natural microenvironment for ICC and GIST; in human GIST cells [10,16], and in LX-2 human hepatic stellate cells [24], a model for cancer niches [25]. The gene discussed is KITLG; the disease is cancer.