The skin is our body’s largest natural barrier, and daily, it undergoes numerous challenges, such as physical injury, chemical insults, and UV radiation. The significance of repairing breaches of this barrier as quickly as possible is especially highlighted in chronic nonhealing wounds, including those associated with diabetes, which affects one in ten people worldwide, with vascular disease and aging. Dying cells in the wound perpetuate inflammation, contribute to dysregulated tissue repair, and increase the risk of infection. Cutaneous wound healing typically consists of four phases, which are hemostasis, inflammation, growth, re-epithelialization, and remodeling. In this chapter, we will discuss how various cell types, immune and nonimmune cells that reside in the epidermis and dermis, die from apoptosis and how efficient dead cell clearance by professional and nonprofessional phagocytes contributes to effective skin wound healing. We will also consider a range of cell death modalities, such as ferroptosis, necroptosis, pyroptosis, and others, and present our current knowledge about their contribution to skin injury and repair.