## 3 Results
### Locus and Genotype of the AKT1 Gene and Psychosis  
The presence of specific molecular genetic variants may, together with environmental risk factors such as cannabis use, contribute to the onset of mental illnesses such as psychosis (schizophrenia), depression and anxiety to a greater extent. There are other conditions such as the age of onset of consumption and the amount consumed that influence the risk of developing a psychotic disorder [10, 14, 22].  
Various studies identify the rs1130233 locus of the AKT1 gene as a modulator of sensitivity to the psychotomimetic effects of cannabis, increasing in people carrying the AKT1 rs1130233 G/G genotype, and producing greater striatal activation affecting cognition after consumption [16, 17, 18, 19]. Likewise, there is a single nucleotide polymorphism (SNP) in the AKT1 gene (rs2494732), which, by interacting with cannabis, moderates the risk of psychosis and short-term psychotomimetic effects, thus simulating prodromes, namely, symptoms before the onset of the disease [20, 21, 22, 23, 24, 25, 26, 27].  
Regarding the risk of onset of psychotic disorder, studies show the presence of the genetic polymorphism of AKT1 rs2494732: homozygotes T/T, heterozygotes C/T and homozygotes C/C [23, 28]. Subjects carrying both alleles without \"risk\", that is, T/T homozygotes of the rs2494732 polymorphism of the AKT1 gene, despite consuming marijuana daily or on weekends, do not increase the probability of onset of psychosis [10, 29, 30, 31]. Likewise, subjects carrying one of the \"risk\" alleles, that is, C/T heterozygotes of the rs2494732 polymorphism of the AKT1 gene, do not present an increased risk of acquiring the psychotic  
\begin{table}
\begin{tabular}{l c c c c c c c} \hline \hline  & **SCOPUS** & **WOS** & **COCHRANE LIBRARY** & **TRIP DATABASE** & **PUBPSYCH** & **PUMBMED** & **TOTAL** \\ \hline Without filters & 33 & 47 & 7 & 12 & 18 & 24 & **141** \\ \hline Duplicates & 0 & 21 & 1 & 5 & 9 & 21 & **57** \\ \hline Other languages & 0 & 0 & 0 & 0 & 0 & 1 & **0** \\ \hline Title and abstract & 10 & 15 & 3 & 7 & 4 & 0 & **39** \\ \hline
**TOTAL VALID** & **23** & **11** & **4** & **0** & **5** & **2** & **45** \\ \hline \hline \end{tabular}
\end{table}
Table 4: Article selection process.  
disorder after consumption [18; 32]. In contrast, based on results obtained, subjects carrying both \"risk\" alleles\", that is, homozygotes C/C of the genetic polymorphism rs2494732 in AKT1, have more than twice the risk of developing psychosis if they are daily users of cannabis as opposed to consumers on weekends, in which the risk is not high [19; 31; 32; 33].  
Similarly, the data show that subjects with two copies of the C allele have a seven-fold increased risk of psychosis compared to subjects with two copies of the T allele, despite considering all subjects' daily cannabis use [27; 34]. In addition, research reveals that selective alterations that lead to sustained attention deficit occur in homozygotes C/C. This increased susceptibility also appears with the muscarinic receptor represented by rs115455482 and rs74722579, which until relatively recently were not identified [20; 33; 34; 35; 36].  
Because cannabis use is a modifiable risk factor, it has been identified that in young people aged between 12 and 21 years old with the rs2494732 polymorphism, and who also have a high family risk of psychotic disorders, genetic counseling is especially useful to enhance the improvement of these individuals' mental health [33; 37; 38].