and decreased concentrations of serum insulin-like growth factor and this was speculated to cause the prolonged cell cycle and hypoplasia seen in the KO mice (Stoffel et al., 2005). Further study showed that the defects seen in the nSMase2 KO mouse were completely rescued via transgenic expression of nSMase2 (Stoffel et al., 2007). Importantly, these data gave essential insight into the potential functional roles of nSMase2.
