Results revealed a significant effect of genotype on the pAkt/Akt ratio, which was lowest in the AA risk variant and highest in the GG nonrisk variant (AA [N=9]: 0.16 [SD=0.10]; AG [N=38]: 0.19 [SD=0.12]; GG [N5=3]: 0.32 [SD=0.19]). A oneway analysis of variance revealed a significant main effect of genotype (F=8.55, df=1, 97, p<0.001; Scheffé's test: AA<GG, AG<GG, p<0.05). This suggests that the CACNA1C risk geno-type is associated with the lowest level of Akt-pathway activation. Intracellular calcium may be involved in Akt activation, and functional polymorphisms of the CACNA1C gene may have an influence on this process. Both mechanisms may be included in memory processes and synaptic plasticity in the hippocampus (5, 8). However, at this time it is not known how rs1006737 affects CAv1.2 functions and whether this polymorphism is causally linked to mental disorders.