In vivo mice models with PTEN homozygous deletion have shown dramatic regression of the Cowden phenotype features of trichilemmomas on treatment with the mTOR (downstream from AKT) inhibitor rapamycin.17 In humans, Hyman et al9 demonstrated that tumor response to targeted treatment with capivasertib was proportional to AKT1 mutation clonality. The gene discussed is AKT1; the disease is neoplasm.