Based on our in vivo and in vitro studies, we speculate that in our model, the crosstalk between epithelial cells and the tumor environment (particularly immune cells) arises mainly via classical paracrine signaling (release of cytokines, chemokines, growth factors and other mediators) initiated by MCPIP1-deficient keratinocytes. The gene discussed is ZC3H12A; the disease is neoplasm.