AXL and melanoma: These adaptive mechanisms exploit the developmental plasticity of melanoma cells and often result in an undifferentiated state characterized by upregulation of receptor tyrosine kinases (RTK) such as PDGFRβ or AXL, downregulation of melanocyte differentiation transcription factors MITF and SOX10 (Sun et al, 2014), and acquisition of mesenchymal and invasive features (Nazarian et al, 2010; Villanueva et al, 2010; Girotti et al, 2013; Muller et al, 2014; Fallahi‐Sichani et al, 2017; Rambow et al, 2018; Tsoi et al, 2018; Rathore et al, 2019).