This study also indicated that ubiquitination‐mediated AKT membrane recruitment does not result from PIP3 binding.80 Apart from this, K14 residue within the PIP3‐binding domain of AKT is required for its with PIP3, which is evident from the inability of binding of mutant (K14R) AKT with PIP3.77, 81, 82 The expression of TRAF2, an E3 ligase, is up‐regulated in the failing heart and its overexpression enhances cardiac hypertrophy and ventricular dysfunction by activating AKT/GSK3β signalling.83 The gene discussed is AKT1; the disease is cardiac hypertrophy.