Taken together, these observations suggest the presence of a potential feedforward loop, whereby loss of APC and activation of β-catenin may trigger STAT3-mediated overexpression of MIR21, and subsequent MIR21-dependent downregulation of JAM-A; this hypothesis is supported by the fact that two of the CRC cell lines with the highest MIR21 expression (HCT116 and Caco-2) have activating mutations in β-catenin. The gene discussed is F11R; the disease is colorectal carcinoma.