Rezatapopt demonstrates the ability to restore function to a specific p53 mutation (Y220C) found in roughly 100,000 cancer patients annually. This small-molecule drug works by stabilizing the mutant protein's structure, allowing it to resume its tumor suppressor role. Early safety data from this Phase 1 trial establishes dosing parameters for larger efficacy studies. The approach represents a significant departure from traditional cancer therapeutics that broadly attack dividing cells. Instead of cytotoxic chemotherapy, rezatapopt specifically targets the molecular defect driving tumor growth. This precision could theoretically benefit patients with solid tumors harboring this particular mutation while sparing healthy tissue. The Y220C variant accounts for roughly 5% of all p53 mutations, making it among the most common single-nucleotide changes in human cancer. However, several critical questions remain unanswered. The Phase 1 design prioritizes safety over efficacy measurement, so tumor response data remains limited. Additionally, p53 reactivation strategies have historically struggled with the protein's complex downstream effects and potential for inducing severe side effects in normal cells that also depend on p53 function.