AKT1 and neoplasm: Additionally, performing MRPS16 knocking down and overexpressing in H23 and H2030 cells, respectively, for the purpose of validating the ability of MRPS16 to promote tumour growth further through PI3K/AKT pathway activation indicated that PI3K (p‐PI3K) and AKT (p‐AKT) phosphorylation levels, not the total PI3K and AKT, besides MCM7 and PCNA proliferation‐related proteins were downregulated by MRPS16 knocking down while promoted by MRPS16 overexpression (Figure 4A), indicating that MRPS16 activates the PI3K/AKT pathway.