Chronic wounds are considered a silent epidemic that impact millions of human lives worldwide, causing comorbidities, reducing life quality and expectancy. Diabetic, pressure, and venous ulcers are the three major clinical entities of chronic wounds, in which the presence of a chronicity phenotype and episodes of recurrence remain as contemporary challenges. We are, accordingly, far from a full understanding about the potential endogenous, predisposing factors that may drive both chronicity and recurrence. Decades of academic and financial endeavors have not translated into a pharmacological intervention that may curb these events. These wounds may exhibit the clinical aspect of a torpid granulative response, poor angiogenesis, delayed or abnormal re-epithelialization, and low contraction rates. At the cellular level, chronicity is propelled and distinguished by the triad of interplaying loops of inflammation, oxidative stress, and cellular senescence. Although the proximal molecular drivers of chronicity and their hierarchal debut sequence are a critical research target and pending task, our unifying hypothesis behind chronicity and recurrence is founded on the existence of an epigenetic pathologic code that originates and perpetuates a "chronic wound memory". In vitro studies suggest that this edited script is sheltered in dermal fibroblasts and keratinocytes and is spreadable and transmissible to descendant cells, dictating abnormal traits even in ideal culture conditions and successive passages. The list of epigenomic alterations and their significance in wound pathology is continuously escalating. The accurate identification of the key epigenetic priming codes of impaired healing, and their selective re-editing, will be remarkably beneficial.