These may include loss-of-function mutations in tumor suppressors (i.e., TP53, Tumor Protein p53; STK11, Serine/Threonine Kinase 11; KEAP1, Kelch-like ECH-associated protein 1), activation of parallel signaling pathways (i.e., PIK3CA, Phosphoinositide 3-kinase mutations), or even a second actionable driver in rare cases, depicted in Figure 1. The gene discussed is TP53; the disease is neoplasm.