Thus, we propose a model for the mode of action of PCLX-001 in B-cell lymphoma whereby inhibition of myristoylation of SFKs (or other proteins including HGAL and Arf1) results not only in a loss of membrane targeting but also in a loss of their protein levels and thus function, via the ubiquitin–proteasome system (Fig.3B), thereby dampening the propagation of BCR signals (Fig. 5). Here, GCSAM is linked to B-cell non-Hodgkin lymphoma.