IL-1β does not encode a typical signal peptide. As a result, newly synthesized pro-IL-1β accumulates within the cytoplasm of activated monocytes and macrophages. The conversion of the inactive pro-IL-1β to its mature form requires the proteolytic action from the IL-1β-converting enzyme (ICE), which is also termed as caspase-1. Secretion of mature IL-1β from LPS-activated monocytes/macrophages is not a constitutive process. These cells must encounter a secondary stimulus that specifically activates the post-translational processing events. Moreover, owing to its pro-inflammatory nature, IL-1β is considered a tumor-promoting cytokine. In fact, enhanced tumor metastasis and angiogenesis have been observed under the influence of IL-1β. IL-1β is able to facilitate tumor progression in murine models of lung cancer. Additionally, the promotion of metastasis and tumor angiogenesis by IL-1β have been associated with increased activity of matrix metalloproteinases and expression of the pro-angiogenic molecule hepatocyte growth factor. IL-1β plays a pathogenic role in Type 1 and Type 2 diabetes, rheumatoid arthritis, and osteoarthritis among other diseases.