It is hypothesized that these cells originate from constitutive activation of the ErbB2/ErbB3 pathway, leading to unregulated activity of PI3K/MEK1 and downstream disruption of adherens junction proteins, notably E-Cadherin.24 This loss of key cell-to-cell interactions has two primary effects in the development of SRCC: (1) formation of a desmoplastic stroma, which facilitates the creation of a tumor growth-enhancing microenvironment, and (2) the generation of the signet ring cell phenotype. The gene discussed is CDH1; the disease is neoplasm.