Since 1980, investigators have developed an increasing number of bacteriophage therapies for the treatment, or prophylaxis, of bacterial infectious diseases [29, 30, 31] . Reports have described that appropriately administered phages can treat lethal infectious diseases caused by gram-negative and gram-positive bacteria, such as Pseudomonas aeruginae, Klebsiella pneumoniae, Enterococcus faecium, and S. aureus [32, 33, 34, 35] . Antibiotic resistance has become a global public health concern; thus investigators are extensively reevalu-ating phage therapies to fully exploit their antimicrobial potential [36, 37] . However, phages encounter a variety of different antiviral mechanisms during their infection of bacterial cells, such as prevention of phage adsorption and DNA entry, cutting of phage nucleic acids, and abortive infection systems [38] . Most reported antiphage systems have been shown to be relevant to the dsDNA phage, but not ssDNA, ssRNA, or dsRNA phages. To further confirm and clarify the first relationship between the TcaR protein and ssDNA phage resistance, the standard plaque assay was performed in E. coli as a model system since little is known about the ssDNA phage infecting Staphylococci. As seen in Figure 5B , induction of the TcaR protein in E. coli conferred increased host resistance to ssDNA phage (M13 and wX174) infection. However, a TcaR-expressing strain did not demonstrate reduced sensitivity to dsDNA phage Lambda (l) infection, suggesting that the phage resistance was caused by TcaR-viral ssDNA complex. The observed biological differences point to a remarkable plasticity of TcaR. These findings, thus, may support a hypothesis that TcaR might interfere with viral ssDNA replication and establish a link between TcaR and ssDNA phage resistance.