MiRNAs promote cell proliferation. MiR-155 and miR-146a were found elevated in HTLV-1-infected cells in vitro. Tax induces the transcription factors NF-κB and AP-1, which promote miR-155 expression by binding the miRNA promoter. This binding resulted in an increased expression of the B-cell integration cluster (BIC) gene whose transcript is processed into miR-155. The interferon regulatory factor-4, IRF4, which is induced in HTLV-1-infected cells, promotes BIC/miR-155 expression. NF-κB also mediates miR-146a transactivation; both miRNAs enhance cellular growth in HTLV-1-infected cells. MiR-150 and miR-223 are differentially regulated in ATLL samples and in HTLV-1-transformed cells. MiR-150 and miR-223 were found upregulated in acute ATLL patients and downregulated in HTLV-1-transformed cell lines. MiR-150 and miR-223 target the STAT1 3′UTR. Inhibition of STAT1 expression, through miR-150, miR-223 reduced proliferation of HTLV-1-transformed and ATLL-derived cell lines. MiR-150 and miR-223, by decreasing STAT1 expression and dampening STAT1-dependent signaling in human T cells, regulated proliferation in an HTLV-1 context.