Exploring host-HTLV-1 interactions and the molecular processes underpinning HTLV-1-mediated carcinogenesis is crucial for establishing effective treatments for viral infection and associated leukemia/lymphoma. Several HTLV-1 proteins have been shown to play important roles in the cellular transformation and immortalization of infected T cells. Through interactions with MAVS, STING, and RIP1, the HTLV-1 oncoprotein Tax suppresses the innate IFN response, resulting in the inhibition of TBK1-mediated phosphorylation of IRF3/IRF7. The HTLV-1 protein HBZ affects genomic integrity and inhibits target cell death and autophagy. Furthermore, it has been discovered that HBZ promotes the growth of ATL cells and aids in the evasion of infected cells from immunosurveillance. It currently appears that the efficacy of an individual's cytotoxic T cell (CTL) response to HTLV-1 is the most important single predictor of that person's provirus load, which can differ by more than 10,000-fold amongst HTLV-1-infected persons. We examine recent improvements in our knowledge of the pathophysiology, or underlying processes, of the illness produced by HTLV-1 infection in this article. Furthermore, we explore the future approach for targeting HTLV-1-associated malignancies and anti-HTLV-1 therapies. The pathogenic agent of adult T-cell leukemia/lymphoma (ATL) is human T-cell lymphotropic virus type 1 (HTLV-1). ATL is a fast-developing clonal tumour of CD4+ T cells which are cellular and viral protein interactions and pave the way for the discovery of new classes of cellular modulators, which may induce Tax oncogenesis and its impact on survival signalling pathways such as the NF-B and PI3K-Akt pathways, therapeutic target opportunities for ATL have been presented in two collaborative studies.