Thus, progression from the Mtb-controlling paucibacillary to non-controlling multibacillary TB lesions in the lungs of TB-susceptible mice was mechanistically linked with a pathological state of macrophage activation characterized by escalating stress (as evidenced by the upregulation of phospho-cJun, PKR, and Chac1), the upregulation of Ifnβ and the IFN-I pathway hyperactivity, with a concurrent reduction of Ifnγ responses. Here, JUN is linked to tuberculosis.