Our data demonstrate that constitutive activation of STAT3 is present in a substantial subset of canine OSA tumors and human and canine cell lines and that downregulation of STAT3 activity through inhibition of upstream Src family kinases using a small molecule inhibitor (SU6656), direct inhibition of STAT3 DNA binding and transcriptional activities using a novel small molecule inhibitor (LLL3), or modulation of STAT3 expression using siRNAs, all resulted in decreased cell proliferation and viability, ultimately inducing caspase-3 mediated apoptosis in treated cells. Here, CASP3 is linked to obstructive sleep apnea syndrome.