Furthermore, the crosstalk between SOCE and mtROS amplifies proinflammatory TNF-α production leading to caspase-8/3 mediated HKM apoptosis and the clearance of M. fortuitum. Our findings elucidate the role of mitochondria in innate immunity to M. fortuitum, which can be used for controlling mycobacteriosis (Figure 6). Here, TNF is linked to mycobacterial infectious disease.