MAP3K8 and familial hyperaldosteronism: However, the increased mortality was only observed in Tpl2 germline knockout FH mice or Tpl2-deficient recipient chimeric FH mice that adoptively transferred with WT BM, but not in the WT recipient chimeric FH mice that adoptively transferred with either WT or Tpl2-deficient BM, suggesting the liver MDSC mobilization during FH pathogenesis is not attributed to the direct intrinsic function of Tpl2 in MDSC, but in hepatocytes.