There could be two logical explanations for this phenomenon, (i) native MARCKS transcript levels increase upon bacterial infection (see Figure 6B) counteracting the effect of the siRNA on MARCKS transcripts and (ii) MARCKS most probably competes with other PKC-η substrates, including MacMARCKS and proteins referred to as STICKs (substrates that interact with C-kinase) (Chapline et al., 1998). Here, MARCKSL1 is linked to bacterial infectious disease.