The former manifests IL-1β, as a driver of inflammation, might lead to innate immune abnormalities to result in the emergence of autoinflammation (31), while the latter is an increase in proliferation of lymphoid T and B cells due to the impact of IL-1β, which possibly increases adaptive immunity, and if this process is excessive, it might lead to the development of AIDs (32). Here, IL1B is linked to AIDS.