Interleukin (IL)‐24, also known as melanoma differentiation‐associated gene‐7, is a cytokine initially identified from cancerous cells and expressed in a range of cell types. It is a regulator of cell differentiation, growth, and apoptosis, and a promising anticancer agent. IL‐24 acts via its heterodimic receptors: the IL‐20R1 and IL‐20R2 complex and the IL‐22R1 and IL‐20R2 complex. There is limited information on the effect of IL‐24 in wound healing. Human acute and chronic wound tissues were used to analyze the transcript levels and histological staining of IL‐24 and the IL‐24 receptors. The biological response of human keratinocytes to recombinant human IL‐24 was evaluated using electric cell‐substrate impedance sensing‐based methods in conjunction with inhibitors to candidate signaling pathways. IL‐24 significantly slowed the migration of keratinocytes (p = 0.01), with only a marginal effect on cellular adhesion. The inhibitory effect of IL‐24 on migration was completed reversed following addition of an AKT inhibitor (p = 0.004) but not an SMAD3 pathway inhibitor. Human chronic wound tissues showed raised levels of both IL‐24 (p = 0.003) and its receptor (p = 0.0305) compared with acute wound tissues. We conclude that IL‐24 appears to promote wound chronicity via its inhibitory effect on the migratory behavior of human keratinocytes, mediated through an AKT‐dependent pathway.