Since cancer cells rely on p53 inactivation for survival through MDM2 overexpression or by gaining p53 mutations, targeting the MDM2‐p53 protein–protein interaction has emerged as a therapeutic strategy to rescue wild type p53.[23] The nine MDM2 inhibitors evaluated in clinical trials[24] mimic three key amino acid residues in the p53 pocket recognized by MDM2, and hence contain several chiral centers with poor synthetic tractability for the extensive trial‐and‐error process necessary to discover a degrader. The gene discussed is TP53; the disease is cancer.