Current evidence points to four interconnected biological mechanisms underlying schizophrenia: dopamine and glutamate neurotransmitter disruption, abnormal prenatal brain development affecting the prefrontal cortex and hippocampus, genetic vulnerabilities identified through genome-wide studies, and immune system dysfunction with inflammatory components. This multi-pathway model explains why dopamine-blocking antipsychotics show limited effectiveness, particularly for cognitive and negative symptoms that significantly impact daily functioning. The convergence of these mechanisms represents a paradigm shift from viewing schizophrenia as primarily a dopamine disorder to understanding it as a complex neurodevelopmental condition with immune components. This broader framework opens therapeutic avenues beyond traditional antipsychotics, including early intervention strategies that target prodromal phases, personalized treatments based on individual genetic and inflammatory profiles, and combination therapies addressing multiple pathways simultaneously. The immune connection is particularly promising, as it suggests anti-inflammatory approaches might complement existing treatments. However, translating this mechanistic understanding into effective therapies remains challenging, requiring biomarkers to identify which patients would benefit from specific pathway-targeted interventions and determining optimal timing for multi-modal treatments.