Given that human PC frequently progresses to an aggressive, therapy-resistant disease characterized by enhanced migratory capacity, stemness, and EMT features [51,52], these observations provide a strong mechanistic rationale for focusing on the integrin–FAK–JNK signaling axis as a key mediator of PDA-induced malignant phenotypic plasticity in PC cells. Here, PTK2 is linked to pachyonychia congenita.