Abstract HTLV-1 is a complex human retrovirus, an etiologic agent in causing malignant and intractable T-cell neoplasia. About 5% of the infected population would progress to acquiring a more aggressive form of non-Hodgkin’s lymphoma (NHL), termed as Adult T-cell leukemia/Lymphoma (ATLL). MEF-2 transcription factors are a family of genes that are involved in distinct functions in various tissues and isoforms of MEF-2 are 2A, 2B, 2C, 2D in mammals whose mutations are implicated in various cancers. Earlier studies from our lab delineated the role of MEF-2A in increased viral gene expression and inhibition of MEF-2A lead to the reduction in HTLV-1 viral replication and associated T-cell transformation. Presently, we have adopted to novel cyto-analytical techniques to quantitate gene transcripts and protein expression patterns at a single cell level for all the MEF-2 isoforms in different cell systems representing productive viral infection and/or ATLL. These studies revealed post-translationally modified, overexpression of MEF-2C and downregulated expression of MEF-2B which are known to be oncogene and tumor suppressor respectively. Similar results were obtained with a unique and specific HDAC-IIa inhibitor namely MC1568, which led to a dose-dependent cancer cell (but not normal) death in vitro while inhibiting viral proteins (Tax and HBZ) expression in vivo. In addition, exposure of HTLV-1-infected cells to MC1568 resulted in the activation of autophagy marker, LC3-II that is currently under investigation to a more in-depth mechanistic analysis.