In the past two decades it has been found that viral proteins might contribute to activation of numerous pathways involved in different types of cancer. Human T-lymphotropic virus 1 (HTLV-1), well known as a cause of T-cell leukemia, was found in patients having different types of cancers. Initiation and development of cancers is usually a multi-year multistep process that starts with initiation of the first somatic mutation and the then the next set of steps with the occurrence of an increasing number of somatic mutations with specific times for each one. Here we suggest a hypothesis: If HTLV-1 virus can infect the nonhematological cell, its viral proteins can work as the agents activating the general cancer-related pathways. This way Tax HTLV-1 protein (and/or other viral proteins) can serve in the similar way as the somatic mutation of specified genes and the presence of Tax can affect the functionality of several pathways that are not yet activated by the timeline of the stages of a "normal" cancer development. For example, the pathways PI3K, p53, TGF-β can be correspondingly be activated and inhibited by Tax before their functional change would appear by the timeline of a "normal" cancer development. The HTLV-1 infection-related KEGG pathway was found when the sets of the most frequently mutated genes for several cancers were analyzed by the DAVID program (that selects the most probable pathways for a set of selected genes). These findings support the hypotheses that HTLV-1 infection can be a common factor in the development of very different cancers, thus warranting further exploration.