Our results concur with the observation that squamous cell carcinoma lines engineered to express constitutively active AKT resulted in the downregulation of the epithelial markers such as E-cadherin.45 Moreover, Ca2+-dependent phosphorylation of AKT following activation of TRPV4 by 4α-PDD is consistent with the report by Danciu et al.46 The group showed that osteoblasts that were uniaxially stretched led to a significant increase in intracellular Ca2+ concentrations resulting in the phosphorylation of PI3K, AKT and its downstream transcription factor targets, FOXO1 and AFX.46 The gene discussed is AKT1; the disease is squamous cell carcinoma.