reported that LDHC4 functions as an oncogene in LUAD, and enhanced LUAD cell growth, proliferation, and tumorigenicity by activating the PI3K/Akt/GSK‐3β pathway.[6] In BC, silencing LDHC in four BC cell lines significantly increased the presence of giant cells, nuclear aberrations, DNA damage, and apoptosis.[29] Our study is the first to investigate the mechanisms of LDHC4 in TNBC from the aspect of metabolic reprogramming. Here, AKT1 is linked to breast cancer.