We have reported that PRKD3 was preferentially overexpressed in breast cancer and involved in promoting the breast cancer progression.2, 12 This study suggested that knocking out PRKD3 led to the inhibition of the breast cancer cell proliferation and tumour growth in vitro and in vivo; however, the ectopic (over)expression of either PRKD3, ERK1 or c‐MYC reversed the inhibition (Figure 5A,B,C and 5). The gene discussed is MYC; the disease is neoplasm.