While activation of some of these proteins is reported to be protective in cardiac disease (heat shock proteins), genetic and pharmacologic manipulation of some others such as JNK/MAPK, Akt1 and PKC has been reported to have conflicting or unknown roles, with both protective and detrimental ramifications for cardiomyocytes after in vitro and in vivo hypoxic injury [34-39]. The gene discussed is AKT1; the disease is heart disorder.