The biological activities of p53(ΔCp44) during HCMV infection remain to be studied, particularly because the p53 C‐terminal sequences reportedly participate in virtually every aspect of p53 function as a transcription factor, including DNA binding, cofactor recruitment, and protein stabilization.1 Understanding how p53(ΔCp44) may participate in HCMV pathogenesis is of interest, as it addresses this and other enigmas, possibly shedding light on currently unrecognized aspects of p53 regulation and function. This evidence concerns the gene TP53 and cytomegalovirus infection.