The article "Inside the genome: understanding genetic influences on oxidative stress" by Hari Krishnan Krishnamurthy et al. explores the genetic factors that influence oxidative stress and its associated diseases. Oxidative stress, defined as an imbalance between oxidants and antioxidants, can lead to cellular damage and various diseases such as cancer, diabetes, and cardiovascular diseases. The authors highlight the roles of both prooxidant and antioxidant genes in maintaining redox balance and their implications in disease states. Prooxidant genes, such as *XDH*, *CYBA*, *CYP1A1*, *PTGS2*, *NOS*, and *MAO*, are involved in generating reactive oxygen species (ROS) and reactive nitrogen species (RNS). Variations in these genes can increase the production of oxidants, leading to oxidative stress. For example, polymorphisms in the *XDH* gene can enhance oxidase function and increase oxidative stress markers. Similarly, polymorphisms in the *CYBA* gene, which encodes NADPH oxidase, can influence NADPH oxidase activity and ROS production. Antioxidant genes, including *SOD*, *CAT*, and *GPX*, encode enzymes that neutralize ROS and RNS, protecting cells from oxidative damage. Polymorphisms in these genes can affect their activity and efficiency, impacting the body's antioxidant defenses. For instance, variations in the *SOD* gene can reduce enzyme activity, increasing susceptibility to oxidative stress. The article also discusses signaling pathways involved in the response to oxidative stress, such as the Nrf2/ARE pathway and the NF-κB pathway. These pathways orchestrate cellular defense mechanisms to restore the balance between oxidants and antioxidants. Additionally, the PI3K/AKT pathway modulates vascular tone by regulating nitric oxide production, highlighting the intricate interplay between oxidative stress and vascular function. Overall, the review emphasizes the importance of understanding the genetics of prooxidants and antioxidants to identify individuals at higher risk of oxidative stress-related diseases and to develop personalized interventions.The article "Inside the genome: understanding genetic influences on oxidative stress" by Hari Krishnan Krishnamurthy et al. explores the genetic factors that influence oxidative stress and its associated diseases. Oxidative stress, defined as an imbalance between oxidants and antioxidants, can lead to cellular damage and various diseases such as cancer, diabetes, and cardiovascular diseases. The authors highlight the roles of both prooxidant and antioxidant genes in maintaining redox balance and their implications in disease states. Prooxidant genes, such as *XDH*, *CYBA*, *CYP1A1*, *PTGS2*, *NOS*, and *MAO*, are involved in generating reactive oxygen species (ROS) and reactive nitrogen species (RNS). Variations in these genes can increase the production of oxidants, leading to oxidative stress. For example, polymorphisms in the *XDH* gene can enhance oxidase function and increase oxidative stress markers. Similarly, polymorphisms in the *CYBA* gene, which encodes NADPH oxidase, can influence NADPH oxidase activity and ROS production. Antioxidant genes, including *SOD*, *CAT*, and *GPX*, encode enzymes that neutralize ROS and RNS, protecting cells from oxidative damage. Polymorphisms in these genes can affect their activity and efficiency, impacting the body's antioxidant defenses. For instance, variations in the *SOD* gene can reduce enzyme activity, increasing susceptibility to oxidative stress. The article also discusses signaling pathways involved in the response to oxidative stress, such as the Nrf2/ARE pathway and the NF-κB pathway. These pathways orchestrate cellular defense mechanisms to restore the balance between oxidants and antioxidants. Additionally, the PI3K/AKT pathway modulates vascular tone by regulating nitric oxide production, highlighting the intricate interplay between oxidative stress and vascular function. Overall, the review emphasizes the importance of understanding the genetics of prooxidants and antioxidants to identify individuals at higher risk of oxidative stress-related diseases and to develop personalized interventions.