Nanomaterials-induced redox imbalance in cancer cells presents significant challenges and opportunities for cancer therapy. Cancer cells exhibit redox imbalance due to increased metabolic activity, mitochondrial dysfunction, and elevated peroxisomal activity, leading to altered gene expression and protein stability. This imbalance can be exploited to trigger programmed cell death and overcome resistance to conventional therapies. Nanotechnology offers new opportunities to modulate redox states in cancer cells through nanomaterials that enhance reactive oxygen species (ROS) production, disrupt antioxidant systems, or both. This review discusses the physiological features of redox imbalance in cancer cells, the challenges in modulating redox states, and the classification of nanomaterials that regulate redox imbalance based on their ability to target redox regulation. It also outlines future perspectives for this field, emphasizing the potential of nanomaterials in cancer therapy, particularly for cancers resistant to radiotherapy or chemotherapy. Cancer cells experience oxidative stress during critical phases of their progression, with mechanisms involving hyperactivation of anabolic pathways, increased mitochondrial function, and oncogenic pathway activation. Cancer cells deploy antioxidant mechanisms to counteract oxidative damage, including glutathione (GSH), thioredoxin (Trx), and antioxidant enzymes. However, antioxidant therapies can stimulate additional malignant phenotypes and increase cancer incidence. Many chemotherapeutic drugs, such as doxorubicin, cisplatin, and arsenic trioxide, kill cancer cells by facilitating ROS accumulation. Despite their efficacy, these agents face challenges due to lack of specificity and systemic toxicity. Nanomaterials can actively respond to local microenvironments and enable precise spatial and temporal functions, offering advantages in cancer therapy. Stimuli-responsive nanomaterials are designed to either directly boost ROS production or disrupt antioxidant defense mechanisms, leading to cell death via apoptosis, autophagy, ferroptosis, or necrosis. These nanomaterials are classified into three categories: 1) inducing excessive reactive oxidative substances under internal or external stimuli; 2) elevating reducing agents to disturb redox balance; 3) combining antioxidant inhibition with ROS/RNS production. Examples include Fenton-like reactions, which generate hydroxyl radicals (·OH) through transition metal elements, and other nanomaterials that generate reactive oxygen species (ROS) or reactive nitrogen species (RNS) under specific conditions. Various nanomaterials have been developed to induce excessive reactive oxidative species, including those that generate ·OH, ^1O2, ·O2^-, and other reactive species. These nanomaterials are designed to respond to internal or external stimuli, such as pH, light, or temperature, to achieve targeted cancer therapy. For example, Fenton-like reactions using iron-based nanomaterials generate ·OH, while other nanomaterials produce ^1O2 or ·O2^- through catalytic reactions. Additionally, nanomaterials that release NO or CO have been developed toNanomaterials-induced redox imbalance in cancer cells presents significant challenges and opportunities for cancer therapy. Cancer cells exhibit redox imbalance due to increased metabolic activity, mitochondrial dysfunction, and elevated peroxisomal activity, leading to altered gene expression and protein stability. This imbalance can be exploited to trigger programmed cell death and overcome resistance to conventional therapies. Nanotechnology offers new opportunities to modulate redox states in cancer cells through nanomaterials that enhance reactive oxygen species (ROS) production, disrupt antioxidant systems, or both. This review discusses the physiological features of redox imbalance in cancer cells, the challenges in modulating redox states, and the classification of nanomaterials that regulate redox imbalance based on their ability to target redox regulation. It also outlines future perspectives for this field, emphasizing the potential of nanomaterials in cancer therapy, particularly for cancers resistant to radiotherapy or chemotherapy. Cancer cells experience oxidative stress during critical phases of their progression, with mechanisms involving hyperactivation of anabolic pathways, increased mitochondrial function, and oncogenic pathway activation. Cancer cells deploy antioxidant mechanisms to counteract oxidative damage, including glutathione (GSH), thioredoxin (Trx), and antioxidant enzymes. However, antioxidant therapies can stimulate additional malignant phenotypes and increase cancer incidence. Many chemotherapeutic drugs, such as doxorubicin, cisplatin, and arsenic trioxide, kill cancer cells by facilitating ROS accumulation. Despite their efficacy, these agents face challenges due to lack of specificity and systemic toxicity. Nanomaterials can actively respond to local microenvironments and enable precise spatial and temporal functions, offering advantages in cancer therapy. Stimuli-responsive nanomaterials are designed to either directly boost ROS production or disrupt antioxidant defense mechanisms, leading to cell death via apoptosis, autophagy, ferroptosis, or necrosis. These nanomaterials are classified into three categories: 1) inducing excessive reactive oxidative substances under internal or external stimuli; 2) elevating reducing agents to disturb redox balance; 3) combining antioxidant inhibition with ROS/RNS production. Examples include Fenton-like reactions, which generate hydroxyl radicals (·OH) through transition metal elements, and other nanomaterials that generate reactive oxygen species (ROS) or reactive nitrogen species (RNS) under specific conditions. Various nanomaterials have been developed to induce excessive reactive oxidative species, including those that generate ·OH, ^1O2, ·O2^-, and other reactive species. These nanomaterials are designed to respond to internal or external stimuli, such as pH, light, or temperature, to achieve targeted cancer therapy. For example, Fenton-like reactions using iron-based nanomaterials generate ·OH, while other nanomaterials produce ^1O2 or ·O2^- through catalytic reactions. Additionally, nanomaterials that release NO or CO have been developed to