In breast cancer cells, hypoxia induces alternative APP splicing linked to breast cancer cell proliferation and tumorigenicity [101] and in non-small cell lung cancer cells, promotes Clk1-dependent Srp55 splicing factor phosphorylation, resulting in alternative VEGFA165b splicing and autonomous growth of VEGFR2 and neuropilin-1 receptor expressing tumour cells [102, 103]. This evidence concerns the gene CLK1 and neoplasm.