These findings expanded beyond the limited purview of the TB “central dogma,” demonstrating that CD4+ T cells act not only as effectors secreting IFN-γ and TNF but also as homeostatic regulators, orchestrating both pro- and anti-inflammatory immunity, thus leading to a more nuanced understanding of protective immunity against TB disease and a broader understanding of how CD4+ T cells modulate the immune response in reinfection events. The gene discussed is CD4; the disease is tuberculosis.