In turn, KYN may spread inflammation through the bloodstream by eliciting mTOR activation, the expansion of CD4+ T cells at the expense of CD8+ T cells, promotes CD3+CD4−CD8− double-negative (DN) T cell and B cell activation and plasma cell expansion; iii) Rab4A-driven mTOR activation promotes ANA production and GN, while the inactivation of Rab4A in T cells restrains CD98 expression, KYN accumulation, mTOR activation, mitochondrial metabolism and lineage skewing and blocks ANA and anti-phospholipid antibody (aPL) production and GN. The gene discussed is MTOR; the disease is ganglioneuroma.