Recent studies have greatly expanded our understanding of PC disease mechanisms at the molecular level, where MAOA primarily utilizes the ROS-Twist1 axis as a central downstream mediator to trigger multiple cellular and molecular events, including cancer-cell-intrinsic signaling cascades, cancer cell crosstalk with the tumor microenvironment, and stromal reprogramming, to collaboratively foster PC development and progression (Figure 1). The gene discussed is MAOA; the disease is pachyonychia congenita.