Research suggests that TINCR might play a role in ALA-PDT (5-aminolevulinic acid- photodynamic therapy)-induced effects on cSCC; the generation of reactive oxygen species (ROS) induced apoptosis and autophagy in tumoral cells via activation of the ERK1/2 pathway, which activated a transcription factor binding to TINCR and supporting its overexpression, thus promoting the inhibition of cSCC progression [68]. This evidence concerns the gene MAPK3 and skin squamous cell carcinoma.