Mouse studies preceding the identification of the human PID due to biallelic LAT mutations have revealed the tolerogenic importance of TCR-induced docking PLCγ1 on LAT.121 In particular, mice harboring a homozygous mutation replacing the docking site of PLCγ1 on LAT, i.e., the tyrosine residue at position 136 of LAT, displayed lethal lupus-like autoimmunity. This evidence concerns the gene LAT and pelvic inflammatory disease.