As SHIP1 agonism did not prevent the LRBA KO mice from succumbing, this could be due to the inability of SHiP1 agonism to mitigate the loss of CTLA4 function in T cells or diminished ILC3 function (e.g., IL17 and IL22 production) or possibly some other immune dysfunction that contributes to lethal disease in the context of a chemically compromised gut epithelial barrier. This evidence concerns the gene INPP5D and immune system disorder.