We performed a separate analysis for the TAIL and the IDOL sequences ( Figures 6A-6D) . The study was performed on all the families that have at least 2 Pfam domains (unique or repeated). The average TAIL in viral proteins is 14 amino acids while the metazoan protein TAIL length is 85 amino acids (p-value,1.0e-150, Figures 6A-6B ). Trimming of protein tails at both termini often leads to a loss of cellular localization signals (e.g., KDEL, PDZ binding sites are found at C-termini) [17] . Importantly, the average IDOL length of the viral proteins in the Pfam families is 30 amino acids, while, for the metazoan equivalent proteins, the length is 67 amino acids (p-value,1.0e-150, Figures 6C-6D) . While a short TAIL may be explained by the viruses having acquired a fragmented sequence from their hosts, the same trend was found for the IDOL. Figure 6C shows that while only 54% of the metazoa IDOL have a length of ,40 amino acids, in the viral proteins from the same Pfam families, 96% of the proteins have IDOL that are shorter than 40 amino acids. These results are consistent with an active trimming and refinement process throughout viral evolution. Short IDOL length is advantageous in suppressing protein misfolding, and hence, improving translation effectiveness [46] . Similarly to the finding of short IDOL sequences in viral proteins, we identified instances of an internal domain which is missing in the viral protein while the flanking domains are maintained in the same order in the eukaryotic homologous protein ( Figure 6E) . The viral putative phosphatidylinositol kinase L615 (UniProt: Q5UR69) is a 701 amino acid protein from the Acanthamoeba polyphaga Mimivirus (APMV) that infects Amoeba. It has two Pfam domains: FYVE (PF01363) followed by PI3_PI4_kinase (PF00454). There are no other known proteins with identical domain architecture in the Amoebozoa kingdom (there are 7 such proteins in other kingdom, e.g., Stramenopiles and Excavata). However, there are 3 proteins from the genus Dictyosteliida (slime molds) that do belong to the Amoebozoa kingdom (UniProt D3BQ22, Q54UU9 and EGC34678). In all 3 of these proteins, the architecture is composed of FYVE domain followed by PI3Ka and PI3_PI4_kinase. The missing domain of PI3Ka in the Mimivirus (APMV) provides an evidence for an active elimination of an internal domain based on parsimonious argument. The findings of shorter IDOL (Figures 6C-6D) or absence of internal domains ( Figure 6E ) are probably the result of the trimming and shortening of the sequences after their acquisition by the virus. The possibility of a domain insertion in eukaryotes cannot be excluded.