In addition, previous findings suggest that EIF3H can interact with and stabilize OGT, enhancing its activity in a deubiquitinase‐dependent manner.[65] This mechanism may similarly operate in obesity‐driven TNBC, amplifying OGT activity and YAP O‐GlcNAcylation through the hexosamine biosynthetic pathway. The gene discussed is OGT; the disease is obesity due to melanocortin 4 receptor deficiency.