On sickle cell anemia, there are a few cases to consider. There are the people that are unaffected, ie, their hemoglobin is a normal shape. In the affected people, in which one amino acid in the hemoglobin protein molecule monomer is changed (hemoglobin is a tetramer of an identical monomer that associates with a haem molecule), causing a large shift in shape of hemoglobin, and the red blood cell, which leads to loss of function (as we all know, hemoglobin is essential for oxygen transport in the body). There are two copies of each chromosome in human cells, and therefore two copies of the hemoglobin gene. One copy is inherited from the mother, and the other one inherited from the father. This means that a person can inherit a good copy from the mother or father, and a bad copy from the other parent, or inherit two bad copies of the gene. Those who inherit 2 bad copies (homozygous for the sickle cell trait) rarely live past adolescence. However, those who have one good copy and one bad copy (heterozygous for the sickle cell trait) still have ~60% functional hemoglobin, and can survive well into adulthood.
People who are homozygous for the dominant normal hemoglobin gene are susceptible to malaria infection, which is caused by flagellate parasites that infect red blood cells. People who are homozygous for the recessive sickle cell trait are resistant to the parasite since it cannot infect red blood cells of sickle shape, but do not have adequate oxygen transport due to the lack of hemoglobin function. However, heterozygotes, or people who have one normal hemoglobin gene, and one sickle cell gene are resistant to malarial infection, and can sufficiently transport oxygen with their one good gene. The reason the deadly sickle cell gene is still around, is that it is selected for in areas where malaria is rampant, such as Africa.