The specific defects observed in fungus-induced ROS production and primary granule release, which are processes known to be selectively governed by p40phox and RAC2, respectively (58, 59, 64–66), prompted investigations that uncovered the detrimental role of BTK inhibition in the activation of p40phox and RAC2 in human neutrophils, revealing the molecular mechanisms of BTKi-driven aspergillosis susceptibility. This evidence concerns the gene BTK and aspergillosis.