CJ affects Notch trafficking, reducing the cell surface expression of N1-TM and preventing the formation of cleaved N1-ICD modules, which results in the transcriptional suppression of Notch1 target genes, such as MYC and HES1. De Ford and colleagues also showed that CJ was more active against HD-mutated T-ALL cells than against a cell line carrying a NOTCH1 juxtamembrane mutation, such as Jurkat [188]. This evidence concerns the gene NOTCH1 and acute lymphoblastic leukemia.