Indeed, SFK mutations known to induce oncogenic activation are extremely rare in PC (0/491 cases in TCGA Firehose), and thus, our development of the Akap12/Rb-null transgenic PC model was meant to genocopy the oncogenic activation of SFK, given AKAP12’s role as a Src scaffolding protein [13] and our finding that AKAP12 loss and LYN gain co-occur in TCGA datasets. This evidence concerns the gene RB1 and pachyonychia congenita.