CBLB and Hepatic fibrosis: Tong et al. found that ubiquitin ligases CBL and CBL-B mutations enhanced FLT3-mTOR signaling by the mechanism that CBL and CBL-B mutations caused them to lose the function of ubiquitinating degradation of FLT3, and the upregulation of FLT3 expression enhanced FLT3-mTOR signaling, allowing more CD8 alpha(+)/CD103(+) DCs (cDC1s) to infiltrate into liver tissues, secrete large amounts of inflammatory factors and chemokines, and exacerbate hepatic fibrosis 91.