Thus, the loss of the kinase-independent function of FAK in cKO-Wnt1 mice, but not cKD-Wnt1 or Ctrl-Wnt1, which could compromise the ability of MMTV-Wnt1 induced expansion of MaSCs, may explain the trend for the delayed tumor initiation times in cKO-Wnt1 tumors relative to cKD-Wnt1 and Ctrl-Wnt1 tumors. The gene discussed is WNT1; the disease is neoplasm.