Remarkably, one of the new forms selectively impairs cellular responses to IL-23 and underlies TB or MSMD in homozygotes, confirming our previous findings implicating the IL-23 pathway in the pathogenesis of mycobacterial disease in patients with IL-23R deficiency or homozygosity for TYK2 P1104A (Fieschi and Casanova, 2003; Boisson-Dupuis et al., 2018; Martinez-Barricarte et al., 2018; Kerner et al., 2019; Boisson-Dupuis and Bustamante, 2021; Casanova and Abel, 2022). This evidence concerns the gene IL23R and Mendelian susceptibility to mycobacterial diseases.