Background: Cancer remains a global health challenge, characterized not just by uncontrolled cell proliferation but also by the complex metabolic reprogramming that underlies its development and progression. Objectives: This review delves into the intricate relationship between cancer and its metabolic alterations, drawing an innovative comparison with the cosmological concepts of dark matter and dark energy to highlight the pivotal yet often overlooked role of metabolic reprogramming in tumor evolution. Methods: It scrutinizes the Warburg effect and other metabolic adaptations, such as shifts in lipid synthesis, amino acid turnover, and mitochondrial function, driven by mutations in key regulatory genes. Results: This review emphasizes the significance of targeting these metabolic pathways for therapeutic intervention, outlining the potential to disrupt cancer’s energy supply and signaling mechanisms. It calls for an interdisciplinary research approach to fully understand and exploit the intricacies of cancer metabolism, pointing toward metabolic reprogramming as a promising frontier for developing more effective cancer treatments. Conclusion: By equating cancer’s metabolic complexity with the enigmatic nature of dark matter and energy, this review underscores the critical need for innovative strategies in oncology, highlighting the importance of unveiling and targeting the “dark energy” within cancer cells to revolutionize future therapy and research.

Hepatocellular carcinoma (HCC) is the most common form of liver cancer, accounting for 80% of cases worldwide. While chronic hepatitis B and C infections remain primary risk factors, emerging evidence highlights the increasing contributions of metabolic dysfunction‐associated steatotic liver disease (MASLD) and alcohol‐associated liver disease (ALD) to HCC development. Genetic predispositions play a crucial role in modulating individual susceptibility to HCC, particularly through variants affecting viral persistence, lipid metabolism, and fibrogenesis. This review aims to summarize key genetic variants associated with precancerous conditions leading to HCC. The genetic risk factors, such as TP53 R249S mutant, TERT promoter mutations, and Wnt/B‐catenin pathway alterations, influence disease progression and treatment response in HCC subjects with chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infections. In MASLD‐related HCC, variants in PNPLA3, TM6SF2, and MBOAT7 modulate hepatic lipid metabolism and fibrosis. ALD‐associated HCC is influenced by polymorphisms in ADH1B, ADH1C, and ALDH2, which affect alcohol metabolism and oxidative stress. Additionally, inherited metabolic disorders, including Wilson's disease and hemochromatosis, further contribute to HCC susceptibility. Despite previous insights into HCC‐related genetic cues, challenges such as limited population‐specific data, lack of genetic screening programs, and ethical concerns regarding genetic tests hinder the translation of genetic discoveries into personalized HCC prevention strategies. Expanding population‐specific studies, improving genetic screening accessibility, and developing standardized risk prediction models will be crucial in shifting traditional medications toward a precision medicine setting for HCC management.

Background and Aims: Metabolic dysfunction–associated steatotic liver disease (MASLD) is an escalating public health concern in East and Southeast Asia, driven by rapid urbanization, dietary transitions, and rising rates of obesity, diabetes, and hypertension. Unique metabolic and phenotypic characteristics among Asian populations, coupled with resource constraints, contribute to underdiagnosis and delayed management. This narrative review aims to examine the burden, risk factors, population‐specific challenges, and public health gaps related to MASLD across East and Southeast Asian countries. Methods: A comprehensive literature search was conducted using PubMed, ScienceDirect, and Google Scholar for studies published from 2010 to 2024. Search terms included “MASLD,” “MAFLD,” “NAFLD,” “fatty liver disease,” “East Asia,” “Southeast Asia,” “risk factors,” and “public health.” Eligible studies included original research, cohort studies, reviews, and meta‐analyses focused on MASLD or NAFLD in the specified regions. Data were synthesized thematically, emphasizing prevalence patterns, lifestyle determinants, vulnerable populations, and health‐system challenges. Results: MASLD prevalence varies widely across East and Southeast Asia, with higher rates observed in urban and high‐income settings. Beyond metabolic drivers, environmental factors, dietary shifts, and socioeconomic disparities strongly influence disease patterns. Distinct subpopulations—including children, older adults, individuals with lean MASLD, and those with chronic comorbidities—experience unique vulnerabilities, often compounded by limited region‐specific data. Major health‐system gaps include inadequate integration of MASLD into primary care, variability in diagnostic access, insufficient public health surveillance, and low provider awareness. Conclusion: MASLD represents a growing yet underrecognized public health issue in East and Southeast Asia. Addressing diagnostic gaps, enhancing primary care capacity, and integrating MASLD within existing metabolic disease programs are essential for improving early detection and long‐term outcomes. Region‐specific strategies and strengthened health systems are critical to mitigating the future burden of MASLD across diverse Asian populations.

Upon further reflection and in consultation with her academic advisors, Ms