I.v. injection of D39, but not PLN-A, into mice caused translocation of PKCα and PKCβII to the membrane compartments of murine cardiomyocytes suggesting activation of these Ca2+-dependent PKC isoforms (Fig 9A and 9B), whereas Ca2+-insensitive PKCs were not affected (S3B Fig), highlighting the pivotal role Ca2+ overload in mediating the activation of these detrimental signalling pathways in vivo subsequent to pneumococcal infection. This evidence concerns the gene PRRT2 and pneumococcal infection.