Moreover, RORγ/RORγT and SPPL2a deficiencies, both underlying MSMD, impair IFN-γ production by TH1* cells (also known as TH1/17 cells), a CCR4−CCR6+CXCR3+ subset of CD4+ αβ T helper cells that typically responds to mycobacterial antigens (42–44), suggesting that human TH1* cells play an essential role in antimycobacterial immunity. This evidence concerns the gene SPPL2A and Mendelian susceptibility to mycobacterial diseases.