ERK1/c‐MYC axis was identified as a major pivot in PRKD3‐regulated pathways in tumour cells.2, 12 However, the interaction mechanisms among PRKD3, ERK1 and c‐MYC in cancer cells has not been well‐investigated since only one prostate cancer study suggested PRKD3‐activated ERK1/2 is involved in tumour growth.13 This evidence concerns the gene MAPK3 and prostate carcinoma.