While hotspot TP53 mutants have been reported to contribute to the chronic inflammation that underlies the development of cancer through cooperation with NF-κB, we have found that SaOS-R273H regulated more inflammation-related genes than SaOS-R175H, including hallmarks of TNF-α (Log P = −4.18) and IL-2 STAT-5 signaling (Log P = −1.9) (Figure 1L,M). The gene discussed is TNF; the disease is cancer.